A chronic, relapsing, inflammatory, and often febrile multisystemic disorder of connective tissue, characterized principally by involvement of the skin, joints, kidneys, and serosal membranes. It is of unknown etiology, but is thought to represent a failure of the regulatory mechanisms of the autoimmune system. The disease is marked by a wide range of system dysfunctions, an elevated erythrocyte sedimentation rate, and the formation of LE cells in the blood or bone marrow.
A chronic form of cutaneous lupus erythematosus (LUPUS ERYTHEMATOSUS, CUTANEOUS) in which the skin lesions mimic those of the systemic form but in which systemic signs are rare. It is characterized by the presence of discoid skin plaques showing varying degrees of edema, erythema, scaliness, follicular plugging, and skin atrophy. Lesions are surrounded by an elevated erythematous border. The condition typically involves the face and scalp, but widespread dissemination may occur.
A form of lupus erythematosus in which the skin may be the only organ involved or in which skin involvement precedes the spread into other body systems. It has been classified into three forms - acute (= LUPUS ERYTHEMATOSUS, SYSTEMIC with skin lesions), subacute, and chronic (= LUPUS ERYTHEMATOSUS, DISCOID).
Glomerulonephritis associated with autoimmune disease SYSTEMIC LUPUS ERYTHEMATOSUS. Lupus nephritis is histologically classified into 6 classes: class I - normal glomeruli, class II - pure mesangial alterations, class III - focal segmental glomerulonephritis, class IV - diffuse glomerulonephritis, class V - diffuse membranous glomerulonephritis, and class VI - advanced sclerosing glomerulonephritis (The World Health Organization classification 1982).
Autoantibodies directed against various nuclear antigens including DNA, RNA, histones, acidic nuclear proteins, or complexes of these molecular elements. Antinuclear antibodies are found in systemic autoimmune diseases including systemic lupus erythematosus, Sjogren's syndrome, scleroderma, polymyositis, and mixed connective tissue disease.
Antibodies that react with self-antigens (AUTOANTIGENS) of the organism that produced them.
Central nervous system vasculitis that is associated with SYSTEMIC LUPUS ERYTHEMATOSUS. Clinical manifestations may include DEMENTIA; SEIZURES; CRANIAL NERVE DISEASES; HEMIPARESIS; BLINDNESS; DYSPHASIA; and other neurological disorders.
A chemotherapeutic agent that acts against erythrocytic forms of malarial parasites. Hydroxychloroquine appears to concentrate in food vacuoles of affected protozoa. It inhibits plasmodial heme polymerase. (From Gilman et al., Goodman and Gilman's The Pharmacological Basis of Therapeutics, 9th ed, p970)
Antiphospholipid antibodies found in association with systemic lupus erythematosus (LUPUS ERYTHEMATOSUS, SYSTEMIC;), ANTIPHOSPHOLIPID SYNDROME; and in a variety of other diseases as well as in healthy individuals. The antibodies are detected by solid-phase IMMUNOASSAY employing the purified phospholipid antigen CARDIOLIPIN.
Inbred NZB mice are a strain of laboratory mice that spontaneously develop an autoimmune disease similar to human systemic lupus erythematosus (SLE), characterized by the production of autoantibodies, immune complex deposition, and glomerulonephritis.
Autoantibodies directed against phospholipids. These antibodies are characteristically found in patients with systemic lupus erythematosus (LUPUS ERYTHEMATOSUS, SYSTEMIC;), ANTIPHOSPHOLIPID SYNDROME; related autoimmune diseases, some non-autoimmune diseases, and also in healthy individuals.
Endogenous tissue constituents that have the ability to interact with AUTOANTIBODIES and cause an immune response.
The presence of antibodies directed against phospholipids (ANTIBODIES, ANTIPHOSPHOLIPID). The condition is associated with a variety of diseases, notably systemic lupus erythematosus and other connective tissue diseases, thrombopenia, and arterial or venous thromboses. In pregnancy it can cause abortion. Of the phospholipids, the cardiolipins show markedly elevated levels of anticardiolipin antibodies (ANTIBODIES, ANTICARDIOLIPIN). Present also are high levels of lupus anticoagulant (LUPUS COAGULATION INHIBITOR).
Disorders that are characterized by the production of antibodies that react with host tissues or immune effector cells that are autoreactive to endogenous peptides.
The major immunoglobulin isotype class in normal human serum. There are several isotype subclasses of IgG, for example, IgG1, IgG2A, and IgG2B.
A mouse substrain that is genetically predisposed to the development of systemic lupus erythematosus-like syndrome, which has been found to be clinically similar to the human disease. It has been determined that this mouse strain carries a mutation in the fas gene. Also, the MRL/lpr is a useful model to study behavioral and cognitive deficits found in autoimmune diseases and the efficacy of immunosuppressive agents.
A glycoprotein that is important in the activation of CLASSICAL COMPLEMENT PATHWAY. C4 is cleaved by the activated COMPLEMENT C1S into COMPLEMENT C4A and COMPLEMENT C4B.
An antiphospholipid antibody found in association with systemic lupus erythematosus (LUPUS ERYTHEMATOSUS, SYSTEMIC;), ANTIPHOSPHOLIPID SYNDROME; and in a variety of other diseases as well as in healthy individuals. In vitro, the antibody interferes with the conversion of prothrombin to thrombin and prolongs the partial thromboplastin time. In vivo, it exerts a procoagulant effect resulting in thrombosis mainly in the larger veins and arteries. It further causes obstetrical complications, including fetal death and spontaneous abortion, as well as a variety of hematologic and neurologic complications.
The protein components that constitute the common core of small nuclear ribonucleoprotein particles. These proteins are commonly referred as Sm nuclear antigens due to their antigenic nature.
The complex formed by the binding of antigen and antibody molecules. The deposition of large antigen-antibody complexes leading to tissue damage causes IMMUNE COMPLEX DISEASES.
A type of lupus erythematosus characterized by deep dermal or subcutaneous nodules, most often on the head, face, or upper arms. It is generally chronic and occurs most often in women between the ages of 20 and 45.
Disorders of connective tissue, especially the joints and related structures, characterized by inflammation, degeneration, or metabolic derangement.
Process whereby the immune system reacts against the body's own tissues. Autoimmunity may produce or be caused by AUTOIMMUNE DISEASES.
A chronic systemic disease, primarily of the joints, marked by inflammatory changes in the synovial membranes and articular structures, widespread fibrinoid degeneration of the collagen fibers in mesenchymal tissues, and by atrophy and rarefaction of bony structures. Etiology is unknown, but autoimmune mechanisms have been implicated.
Chronic inflammatory and autoimmune disease in which the salivary and lacrimal glands undergo progressive destruction by lymphocytes and plasma cells resulting in decreased production of saliva and tears. The primary form, often called sicca syndrome, involves both KERATOCONJUNCTIVITIS SICCA and XEROSTOMIA. The secondary form includes, in addition, the presence of a connective tissue disease, usually rheumatoid arthritis.
A subcomponent of complement C1, composed of six copies of three polypeptide chains (A, B, and C), each encoded by a separate gene (C1QA; C1QB; C1QC). This complex is arranged in nine subunits (six disulfide-linked dimers of A and B, and three disulfide-linked homodimers of C). C1q has binding sites for antibodies (the heavy chain of IMMUNOGLOBULIN G or IMMUNOGLOBULIN M). The interaction of C1q and immunoglobulin activates the two proenzymes COMPLEMENT C1R and COMPLEMENT C1S, thus initiating the cascade of COMPLEMENT ACTIVATION via the CLASSICAL COMPLEMENT PATHWAY.
Inflammation of any part of the KIDNEY.
Abnormal responses to sunlight or artificial light due to extreme reactivity of light-absorbing molecules in tissues. It refers almost exclusively to skin photosensitivity, including sunburn, reactions due to repeated prolonged exposure in the absence of photosensitizing factors, and reactions requiring photosensitizing factors such as photosensitizing agents and certain diseases. With restricted reference to skin tissue, it does not include photosensitivity of the eye to light, as in photophobia or photosensitive epilepsy.
Levels within a diagnostic group which are established by various measurement criteria applied to the seriousness of a patient's disorder.
A glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states.
A glycoprotein that is central in both the classical and the alternative pathway of COMPLEMENT ACTIVATION. C3 can be cleaved into COMPLEMENT C3A and COMPLEMENT C3B, spontaneously at low level or by C3 CONVERTASE at high level. The smaller fragment C3a is an ANAPHYLATOXIN and mediator of local inflammatory process. The larger fragment C3b binds with C3 convertase to form C5 convertase.
Small RNAs found in the cytoplasm usually complexed with proteins in scRNPs (RIBONUCLEOPROTEINS, SMALL CYTOPLASMIC).
Lymphoid cells concerned with humoral immunity. They are short-lived cells resembling bursa-derived lymphocytes of birds in their production of immunoglobulin upon appropriate stimulation.
A deoxyribonucleotide polymer that is the primary genetic material of all cells. Eukaryotic and prokaryotic organisms normally contain DNA in a double-stranded state, yet several important biological processes transiently involve single-stranded regions. DNA, which consists of a polysugar-phosphate backbone possessing projections of purines (adenine and guanine) and pyrimidines (thymine and cytosine), forms a double helix that is held together by hydrogen bonds between these purines and pyrimidines (adenine to thymine and guanine to cytosine).
Agents that suppress immune function by one of several mechanisms of action. Classical cytotoxic immunosuppressants act by inhibiting DNA synthesis. Others may act through activation of T-CELLS or by inhibiting the activation of HELPER CELLS. While immunosuppression has been brought about in the past primarily to prevent rejection of transplanted organs, new applications involving mediation of the effects of INTERLEUKINS and other CYTOKINES are emerging.
A heterogeneous group of disorders, some hereditary, others acquired, characterized by abnormal structure or function of one or more of the elements of connective tissue, i.e., collagen, elastin, or the mucopolysaccharides.
A class of immunoglobulin bearing mu chains (IMMUNOGLOBULIN MU-CHAINS). IgM can fix COMPLEMENT. The name comes from its high molecular weight and originally being called a macroglobulin.
Studies which start with the identification of persons with a disease of interest and a control (comparison, referent) group without the disease. The relationship of an attribute to the disease is examined by comparing diseased and non-diseased persons with regard to the frequency or levels of the attribute in each group.
An immunoassay utilizing an antibody labeled with an enzyme marker such as horseradish peroxidase. While either the enzyme or the antibody is bound to an immunosorbent substrate, they both retain their biologic activity; the change in enzyme activity as a result of the enzyme-antibody-antigen reaction is proportional to the concentration of the antigen and can be measured spectrophotometrically or with the naked eye. Many variations of the method have been developed.
A latent susceptibility to disease at the genetic level, which may be activated under certain conditions.
A tumor necrosis factor superfamily member that plays a role in the regulation of B-LYMPHOCYTE survival. It occurs as a membrane-bound protein that is cleaved to release an biologically active soluble form with specificity to TRANSMEMBRANE ACTIVATOR AND CAML INTERACTOR PROTEIN; B-CELL ACTIVATION FACTOR RECEPTOR; and B-CELL MATURATION ANTIGEN.
Acidic phospholipids composed of two molecules of phosphatidic acid covalently linked to a molecule of glycerol. They occur primarily in mitochondrial inner membranes and in bacterial plasma membranes. They are the main antigenic components of the Wassermann-type antigen that is used in nontreponemal SYPHILIS SERODIAGNOSIS.
Historically, a heterogeneous group of acute and chronic diseases, including rheumatoid arthritis, systemic lupus erythematosus, progressive systemic sclerosis, dermatomyositis, etc. This classification was based on the notion that "collagen" was equivalent to "connective tissue", but with the present recognition of the different types of collagen and the aggregates derived from them as distinct entities, the term "collagen diseases" now pertains exclusively to those inherited conditions in which the primary defect is at the gene level and affects collagen biosynthesis, post-translational modification, or extracellular processing directly. (From Cecil Textbook of Medicine, 19th ed, p1494)
A syndrome with overlapping clinical features of systemic lupus erythematosus, scleroderma, polymyositis, and Raynaud's phenomenon. The disease is differentially characterized by high serum titers of antibodies to ribonuclease-sensitive extractable (saline soluble) nuclear antigen and a "speckled" epidermal nuclear staining pattern on direct immunofluorescence.
The smaller fragment formed when complement C4 is cleaved by COMPLEMENT C1S. It is an anaphylatoxin that causes symptoms of immediate hypersensitivity (HYPERSENSITIVITY, IMMEDIATE) but its activity is weaker than that of COMPLEMENT C3A or COMPLEMENT C5A.
Inflammation of a serous membrane.
A chronic multi-system disorder of CONNECTIVE TISSUE. It is characterized by SCLEROSIS in the SKIN, the LUNGS, the HEART, the GASTROINTESTINAL TRACT, the KIDNEYS, and the MUSCULOSKELETAL SYSTEM. Other important features include diseased small BLOOD VESSELS and AUTOANTIBODIES. The disorder is named for its most prominent feature (hard skin), and classified into subsets by the extent of skin thickening: LIMITED SCLERODERMA and DIFFUSE SCLERODERMA.
A form of cutaneous tuberculosis. It is seen predominantly in women and typically involves the NASAL MUCOSA; BUCCAL MUCOSA; and conjunctival mucosa.
Inflammation of the renal glomeruli (KIDNEY GLOMERULUS) that can be classified by the type of glomerular injuries including antibody deposition, complement activation, cellular proliferation, and glomerulosclerosis. These structural and functional abnormalities usually lead to HEMATURIA; PROTEINURIA; HYPERTENSION; and RENAL INSUFFICIENCY.
Complexes of RNA-binding proteins with ribonucleic acids (RNA).
Highly conserved nuclear RNA-protein complexes that function in RNA processing in the nucleus, including pre-mRNA splicing and pre-mRNA 3'-end processing in the nucleoplasm, and pre-rRNA processing in the nucleolus (see RIBONUCLEOPROTEINS, SMALL NUCLEOLAR).
A 44-kDa highly glycosylated plasma protein that binds phospholipids including CARDIOLIPIN; APOLIPOPROTEIN E RECEPTOR; membrane phospholipids, and other anionic phospholipid-containing moieties. It plays a role in coagulation and apoptotic processes. Formerly known as apolipoprotein H, it is an autoantigen in patients with ANTIPHOSPHOLIPID ANTIBODIES.
Measurable and quantifiable biological parameters (e.g., specific enzyme concentration, specific hormone concentration, specific gene phenotype distribution in a population, presence of biological substances) which serve as indices for health- and physiology-related assessments, such as disease risk, psychiatric disorders, environmental exposure and its effects, disease diagnosis, metabolic processes, substance abuse, pregnancy, cell line development, epidemiologic studies, etc.
Serum glycoproteins participating in the host defense mechanism of COMPLEMENT ACTIVATION that creates the COMPLEMENT MEMBRANE ATTACK COMPLEX. Included are glycoproteins in the various pathways of complement activation (CLASSICAL COMPLEMENT PATHWAY; ALTERNATIVE COMPLEMENT PATHWAY; and LECTIN COMPLEMENT PATHWAY).
Inflammation of any one of the blood vessels, including the ARTERIES; VEINS; and rest of the vasculature system in the body.
The property of antibodies which enables them to react with some ANTIGENIC DETERMINANTS and not with others. Specificity is dependent on chemical composition, physical forces, and molecular structure at the binding site.
Lymphocytes responsible for cell-mediated immunity. Two types have been identified - cytotoxic (T-LYMPHOCYTES, CYTOTOXIC) and helper T-lymphocytes (T-LYMPHOCYTES, HELPER-INDUCER). They are formed when lymphocytes circulate through the THYMUS GLAND and differentiate to thymocytes. When exposed to an antigen, they divide rapidly and produce large numbers of new T cells sensitized to that antigen.
Abnormal immunoglobulins, especially IGG or IGM, that precipitate spontaneously when SERUM is cooled below 37 degrees Celsius. It is characteristic of CRYOGLOBULINEMIA.
The presence of proteins in the urine, an indicator of KIDNEY DISEASES.
Adrenal cortex hormones are steroid hormones produced by the outer portion of the adrenal gland, consisting of glucocorticoids, mineralocorticoids, and androgens, which play crucial roles in various physiological processes such as metabolism regulation, stress response, electrolyte balance, and sexual development and function.
Specific molecular sites on the surface of various cells, including B-lymphocytes and macrophages, that combine with IMMUNOGLOBULIN Gs. Three subclasses exist: Fc gamma RI (the CD64 antigen, a low affinity receptor), Fc gamma RII (the CD32 antigen, a high affinity receptor), and Fc gamma RIII (the CD16 antigen, a low affinity receptor).
Procedure whereby plasma is separated and extracted from anticoagulated whole blood and the red cells retransfused to the donor. Plasmapheresis is also employed for therapeutic use.
An immunosuppressive agent used in combination with cyclophosphamide and hydroxychloroquine in the treatment of rheumatoid arthritis. According to the Fourth Annual Report on Carcinogens (NTP 85-002, 1985), this substance has been listed as a known carcinogen. (Merck Index, 11th ed)
A PREDNISOLONE derivative with similar anti-inflammatory action.
A family of transcription factors that share an N-terminal HELIX-TURN-HELIX MOTIF and bind INTERFERON-inducible promoters to control GENE expression. IRF proteins bind specific DNA sequences such as interferon-stimulated response elements, interferon regulatory elements, and the interferon consensus sequence.
A classification of B-lymphocytes based on structurally or functionally different populations of cells.
A single nucleotide variation in a genetic sequence that occurs at appreciable frequency in the population.
The large fragment formed when COMPLEMENT C4 is cleaved by COMPLEMENT C1S. The membrane-bound C4b binds COMPLEMENT C2A, a SERINE PROTEASE, to form C4b2a (CLASSICAL PATHWAY C3 CONVERTASE) and subsequent C4b2a3b (CLASSICAL PATHWAY C5 CONVERTASE).
A synthetic anti-inflammatory glucocorticoid derived from CORTISONE. It is biologically inert and converted to PREDNISOLONE in the liver.
Immunoglobulin molecules having a specific amino acid sequence by virtue of which they interact only with the ANTIGEN (or a very similar shape) that induced their synthesis in cells of the lymphoid series (especially PLASMA CELLS).
A component of the CLASSICAL COMPLEMENT PATHWAY. C2 is cleaved by activated COMPLEMENT C1S into COMPLEMENT C2B and COMPLEMENT C2A. C2a, the COOH-terminal fragment containing a SERINE PROTEASE, combines with COMPLEMENT C4B to form C4b2a (CLASSICAL PATHWAY C3 CONVERTASE) and subsequent C4b2a3b (CLASSICAL PATHWAY C5 CONVERTASE).
Morphologic alteration of small B LYMPHOCYTES or T LYMPHOCYTES in culture into large blast-like cells able to synthesize DNA and RNA and to divide mitotically. It is induced by INTERLEUKINS; MITOGENS such as PHYTOHEMAGGLUTININS, and by specific ANTIGENS. It may also occur in vivo as in GRAFT REJECTION.
A group of CORTICOSTEROIDS that affect carbohydrate metabolism (GLUCONEOGENESIS, liver glycogen deposition, elevation of BLOOD SUGAR), inhibit ADRENOCORTICOTROPIC HORMONE secretion, and possess pronounced anti-inflammatory activity. They also play a role in fat and protein metabolism, maintenance of arterial blood pressure, alteration of the connective tissue response to injury, reduction in the number of circulating lymphocytes, and functioning of the central nervous system.
Antibodies produced by a single clone of cells.
Inflammation of a transverse portion of the spinal cord characterized by acute or subacute segmental demyelination or necrosis. The condition may occur sporadically, follow an infection or vaccination, or present as a paraneoplastic syndrome (see also ENCEPHALOMYELITIS, ACUTE DISSEMINATED). Clinical manifestations include motor weakness, sensory loss, and incontinence. (Adams et al., Principles of Neurology, 6th ed, pp1242-6)
Body organ that filters blood for the secretion of URINE and that regulates ion concentrations.
Antibodies which react with the individual structural determinants (idiotopes) on the variable region of other antibodies.
'Skin diseases' is a broad term for various conditions affecting the skin, including inflammatory disorders, infections, benign and malignant tumors, congenital abnormalities, and degenerative diseases, which can cause symptoms such as rashes, discoloration, eruptions, lesions, itching, or pain.
An aspect of personal behavior or lifestyle, environmental exposure, or inborn or inherited characteristic, which, on the basis of epidemiologic evidence, is known to be associated with a health-related condition considered important to prevent.
The genetic constitution of the individual, comprising the ALLELES present at each GENETIC LOCUS.
A cluster of convoluted capillaries beginning at each nephric tubule in the kidney and held together by connective tissue.
Acquired hemolytic anemia due to the presence of AUTOANTIBODIES which agglutinate or lyse the patient's own RED BLOOD CELLS.
One of the type I interferons produced by peripheral blood leukocytes or lymphoblastoid cells. In addition to antiviral activity, it activates NATURAL KILLER CELLS and B-LYMPHOCYTES, and down-regulates VASCULAR ENDOTHELIAL GROWTH FACTOR expression through PI-3 KINASE and MAPK KINASES signaling pathways.
Naturally occurring or experimentally induced animal diseases with pathological processes sufficiently similar to those of human diseases. They are used as study models for human diseases.
Studies in which subsets of a defined population are identified. These groups may or may not be exposed to factors hypothesized to influence the probability of the occurrence of a particular disease or other outcome. Cohorts are defined populations which, as a whole, are followed in an attempt to determine distinguishing subgroup characteristics.
Technique using an instrument system for making, processing, and displaying one or more measurements on individual cells obtained from a cell suspension. Cells are usually stained with one or more fluorescent dyes specific to cell components of interest, e.g., DNA, and fluorescence of each cell is measured as it rapidly transverses the excitation beam (laser or mercury arc lamp). Fluorescence provides a quantitative measure of various biochemical and biophysical properties of the cell, as well as a basis for cell sorting. Other measurable optical parameters include light absorption and light scattering, the latter being applicable to the measurement of cell size, shape, density, granularity, and stain uptake.
A member of tumor necrosis factor superfamily found on MACROPHAGES; DENDRITIC CELLS and T-LYMPHOCYTES. It occurs as transmembrane protein that can be cleaved to release a secreted form that specifically binds to TRANSMEMBRANE ACTIVATOR AND CAML INTERACTOR PROTEIN; and B CELL MATURATION ANTIGEN.
A subnormal level of BLOOD PLATELETS.
Variant forms of the same gene, occupying the same locus on homologous CHROMOSOMES, and governing the variants in production of the same gene product.
The regular and simultaneous occurrence in a single interbreeding population of two or more discontinuous genotypes. The concept includes differences in genotypes ranging in size from a single nucleotide site (POLYMORPHISM, SINGLE NUCLEOTIDE) to large nucleotide sequences visible at a chromosomal level.
Molecular sites on or in some B-lymphocytes and macrophages that recognize and combine with COMPLEMENT C3B. The primary structure of these receptors reveal that they contain transmembrane and cytoplasmic domains, with their extracellular portion composed entirely of thirty short consensus repeats each having 60 to 70 amino acids.
Individuals whose ancestral origins are in the continent of Europe.
Measurement of rate of settling of erythrocytes in anticoagulated blood.
White blood cells formed in the body's lymphoid tissue. The nucleus is round or ovoid with coarse, irregularly clumped chromatin while the cytoplasm is typically pale blue with azurophilic (if any) granules. Most lymphocytes can be classified as either T or B (with subpopulations of each), or NATURAL KILLER CELLS.
Mature LYMPHOCYTES and MONOCYTES transported by the blood to the body's extravascular space. They are morphologically distinguishable from mature granulocytic leukocytes by their large, non-lobed nuclei and lack of coarse, heavily stained cytoplasmic granules.
Removal and pathologic examination of specimens in the form of small pieces of tissue from the living body.
The proportion of one particular in the total of all ALLELES for one genetic locus in a breeding POPULATION.
Unique genetically-controlled determinants present on ANTIBODIES whose specificity is limited to a single group of proteins (e.g., another antibody molecule or an individual myeloma protein). The idiotype appears to represent the antigenicity of the antigen-binding site of the antibody and to be genetically codetermined with it. The idiotypic determinants have been precisely located to the IMMUNOGLOBULIN VARIABLE REGION of both immunoglobin polypeptide chains.
Test for tissue antigen using either a direct method, by conjugation of antibody with fluorescent dye (FLUORESCENT ANTIBODY TECHNIQUE, DIRECT) or an indirect method, by formation of antigen-antibody complex which is then labeled with fluorescein-conjugated anti-immunoglobulin antibody (FLUORESCENT ANTIBODY TECHNIQUE, INDIRECT). The tissue is then examined by fluorescence microscopy.
A 206-amino-acid fragment in the alpha chain (672-1663) of C3b. It is generated when C3b is inactivated (iC3b) and its alpha chain is cleaved by COMPLEMENT FACTOR I into C3c (749-954), and C3dg (955-1303) in the presence COMPLEMENT FACTOR H.
Antibodies found in adult RHEUMATOID ARTHRITIS patients that are directed against GAMMA-CHAIN IMMUNOGLOBULINS.
Multi-subunit proteins which function in IMMUNITY. They are produced by B LYMPHOCYTES from the IMMUNOGLOBULIN GENES. They are comprised of two heavy (IMMUNOGLOBULIN HEAVY CHAINS) and two light chains (IMMUNOGLOBULIN LIGHT CHAINS) with additional ancillary polypeptide chains depending on their isoforms. The variety of isoforms include monomeric or polymeric forms, and transmembrane forms (B-CELL ANTIGEN RECEPTORS) or secreted forms (ANTIBODIES). They are divided by the amino acid sequence of their heavy chains into five classes (IMMUNOGLOBULIN A; IMMUNOGLOBULIN D; IMMUNOGLOBULIN E; IMMUNOGLOBULIN G; IMMUNOGLOBULIN M) and various subclasses.
The genetic constitution of individuals with respect to one member of a pair of allelic genes, or sets of genes that are closely linked and tend to be inherited together such as those of the MAJOR HISTOCOMPATIBILITY COMPLEX.
Formation and development of a thrombus or blood clot in the blood vessel.
Enzymes that activate one or more COMPLEMENT PROTEINS in the complement system leading to the formation of the COMPLEMENT MEMBRANE ATTACK COMPLEX, an important response in host defense. They are enzymes in the various COMPLEMENT ACTIVATION pathways.
Precursor of an alkylating nitrogen mustard antineoplastic and immunosuppressive agent that must be activated in the LIVER to form the active aldophosphamide. It has been used in the treatment of LYMPHOMA and LEUKEMIA. Its side effect, ALOPECIA, has been used for defleecing sheep. Cyclophosphamide may also cause sterility, birth defects, mutations, and cancer.
An antibiotic substance derived from Penicillium stoloniferum, and related species. It blocks de novo biosynthesis of purine nucleotides by inhibition of the enzyme inosine monophosphate dehydrogenase. Mycophenolic acid is important because of its selective effects on the immune system. It prevents the proliferation of T-cells, lymphocytes, and the formation of antibodies from B-cells. It also may inhibit recruitment of leukocytes to inflammatory sites. (From Gilman et al., Goodman and Gilman's The Pharmacological Basis of Therapeutics, 9th ed, p1301)
A membrane-bound tumor necrosis family member that is expressed on activated antigen-presenting cells such as B-LYMPHOCYTES and MACROPHAGES. It signals T-LYMPHOCYTES by binding the OX40 RECEPTOR.
A signal transducer and activator of transcription that mediates cellular responses to INTERLEUKIN-12 in T-LYMPHOCYTES. Stat4 is an important signaling molecule for differentiation in TH1 CELLS.
Studies used to test etiologic hypotheses in which inferences about an exposure to putative causal factors are derived from data relating to characteristics of persons under study or to events or experiences in their past. The essential feature is that some of the persons under study have the disease or outcome of interest and their characteristics are compared with those of unaffected persons.
Conditions or pathological processes associated with pregnancy. They can occur during or after pregnancy, and range from minor discomforts to serious diseases that require medical interventions. They include diseases in pregnant females, and pregnancies in females with diseases.
Antibodies obtained from a single clone of cells grown in mice or rats.
Pathological processes of the KIDNEY or its component tissues.
A pattern recognition receptor that binds several forms of imidazo-quinoline including the antiviral compound Imiquimod.
Endogenous substances, usually proteins, that are involved in the blood coagulation process.
Pathological conditions in the INTESTINES that are characterized by the gastrointestinal loss of serum proteins, including SERUM ALBUMIN; IMMUNOGLOBULINS; and at times LYMPHOCYTES. Severe condition can result in HYPOGAMMAGLOBULINEMIA or LYMPHOPENIA. Protein-losing enteropathies are associated with a number of diseases including INTESTINAL LYMPHANGIECTASIS; WHIPPLE'S DISEASE; and NEOPLASMS of the SMALL INTESTINE.
Diseases of any component of the brain (including the cerebral hemispheres, diencephalon, brain stem, and cerebellum) or the spinal cord.
Drugs that are used to treat RHEUMATOID ARTHRITIS.
A pattern recognition receptor that binds unmethylated CPG CLUSTERS. It mediates cellular responses to bacterial pathogens by distinguishing between self and bacterial DNA.
Individuals whose ancestral origins are in the southeastern and eastern areas of the Asian continent.
An idiopathic vascular disorder characterized by bilateral Raynaud phenomenon, the abrupt onset of digital paleness or CYANOSIS in response to cold exposure or stress.
Cells propagated in vitro in special media conducive to their growth. Cultured cells are used to study developmental, morphologic, metabolic, physiologic, and genetic processes, among others.
The worsening of a disease over time. This concept is most often used for chronic and incurable diseases where the stage of the disease is an important determinant of therapy and prognosis.
Mouse strains constructed to possess identical genotypes except for a difference at a single gene locus.
Interferon secreted by leukocytes, fibroblasts, or lymphoblasts in response to viruses or interferon inducers other than mitogens, antigens, or allo-antigens. They include alpha- and beta-interferons (INTERFERON-ALPHA and INTERFERON-BETA).
Observation of a population for a sufficient number of persons over a sufficient number of years to generate incidence or mortality rates subsequent to the selection of the study group.
A loss of mucous substance of the mouth showing local excavation of the surface, resulting from the sloughing of inflammatory necrotic tissue. It is the result of a variety of causes, e.g., denture irritation, aphthous stomatitis (STOMATITIS, APHTHOUS); NOMA; necrotizing gingivitis (GINGIVITIS, NECROTIZING ULCERATIVE); TOOTHBRUSHING; and various irritants. (From Jablonski, Dictionary of Dentistry, 1992, p842)
A screening assay for circulating COMPLEMENT PROTEINS. Diluted SERUM samples are added to antibody-coated ERYTHROCYTES and the percentage of cell lysis is measured. The values are expressed by the so called CH50, in HEMOLYTIC COMPLEMENT units per milliliter, which is the dilution of serum required to lyse 50 percent of the erythrocytes in the assay.
The age, developmental stage, or period of life at which a disease or the initial symptoms or manifestations of a disease appear in an individual.
Studies in which individuals or populations are followed to assess the outcome of exposures, procedures, or effects of a characteristic, e.g., occurrence of disease.
Molecules on the surface of some B-lymphocytes and macrophages, that recognize and combine with the C3b, C3d, C1q, and C4b components of complement.
A subtype of non-receptor protein tyrosine phosphatases that is characterized by the presence of an N-terminal catalytic domain and a C-terminal PROLINE-rich domain. The phosphatase subtype is predominantly expressed in LYMPHOCYTES and plays a key role in the inhibition of downstream T-LYMPHOCYTE activation. Polymorphisms in the gene that encodes this phosphatase subtype are associated with a variety of AUTOIMMUNE DISEASES.
Facial dermatoses refers to various skin conditions that affect the face, causing symptoms such as redness, inflammation, papules, pustules, scaling, or pigmentation changes, which can be caused by a range of factors including genetics, infections, allergies, and environmental factors.
Substances that reduce or suppress INFLAMMATION.
Biologically active substances whose activities affect or play a role in the functioning of the immune system.
The sequential activation of serum COMPLEMENT PROTEINS to create the COMPLEMENT MEMBRANE ATTACK COMPLEX. Factors initiating complement activation include ANTIGEN-ANTIBODY COMPLEXES, microbial ANTIGENS, or cell surface POLYSACCHARIDES.
An HLA-DR antigen which is associated with HLA-DRB1 CHAINS encoded by DRB1*03 alleles.
Persons living in the United States having origins in any of the black groups of Africa.
Sites on an antigen that interact with specific antibodies.
Development of lesions in the lymph node characterized by infiltration of the cortex or paracortex by large collections of proliferating histiocytes and complete or, more often, incomplete necrosis of lymphoid tissue.
The outer covering of the body that protects it from the environment. It is composed of the DERMIS and the EPIDERMIS.
Evaluation undertaken to assess the results or consequences of management and procedures used in combating disease in order to determine the efficacy, effectiveness, safety, and practicability of these interventions in individual cases or series.

Fitzgerald factor (high molecular weight kininogen) clotting activity in human plasma in health and disease in various animal plasmas. (1/6365)

Fitzgerald factor (high molecular weight kininogen) is an agent in normal human plasma that corrects the impaired in vitro surface-mediated plasma reactions of blood coagulation, fibrinolysis, and kinin generation observed in Fitzgerald trait plasma. To assess the possible pathophysiologic role of Fitzgerald factor, its titer was measured by a functional clot-promoting assay. Mean +/- SD in 42 normal adults was 0.99+/-0.25 units/ml, one unit being the activity in 1 ml of normal pooled plasma. No difference in titer was noted between normal men and women, during pregnancy, or after physical exercise. Fitzgerald factor activity was significantly reduced in the plasmas of eight patients with advanced hepatic cirrhosis (0.40+/-0.09 units/ml) and of ten patients with disseminated intravascular coagulation (0.60+/-0.30 units/ml), but was normal in plasmas of patients with other congenital clotting factor deficiencies, nephrotic syndrome, rheumatoid arthritis, systemic lupus erythematosus, or sarcoidosis, or under treatment with warfarin. The plasmas of 21 mammalian species tested appeared to contain Fitzgerald factor activity, but those of two avian, two repitilian, and one amphibian species did not correct the coagulant defect in Fitzgerald trait plasmas.  (+info)

Fine specificity of the autoimmune response to the Ro/SSA and La/SSB ribonucleoproteins. (2/6365)

The fine specificity of the Ro and La proteins has been studied by several techniques. In general, there is agreement in a qualitative sense that autoantibodies bind multiple epitopes. For some specific antibody binding, different studies agree quantitatively, for instance, the binding of the carboxyl terminus of 60-kd Ro as described by 2 studies using different techniques and the presence of an epitope within the leucine zipper of 52-kd Ro. In addition, there is general agreement about the location of a prominent epitope at the RRM motif region of the La molecule. On the other hand, the many specific epitope regions of the molecules differ among these studies. These discrepancies are likely the result of using different techniques, sera, and peptide constructs as well as a result of inherent advantages and disadvantages in the individual approaches. Several theories concerning the origin of not only the antibodies, but also the diseases themselves, have been generated from studies of the fine specificity of antibody binding. These include a theory of a primordial foreign antigen for anti-Ro autoimmunity, molecular mimicry with regard to La and CCHB, as well as the association of anti-Ro with HLA. These remain unproven, but are of continuing interest. An explanation for the association of anti-60-kd Ro and anti-52-kd Ro in the sera of patients has sprung from evaluating antibody binding. Data demonstrating multiple epitopes are part of a large body of evidence that strongly suggests an antigen-driven immune response. This means that the autoantigens are directly implicated in initiating and sustaining autoimmunity in their associated diseases. A number of studies have investigated the possibility of differences in the immune response to these antigens in SS and SLE sera. While several differences have been reported, none have been reproduced in a second cohort of patients. Furthermore, none of the reported differences may be sufficiently robust for clinical purposes, such as distinguishing between SS with systemic features and mild SLE, although some might be promising. For instance, in at least 3 groups of SLE patients, no binding of residues spanning amino acids 21-41 of 60-kd Ro has been found. Meanwhile, 1 of those studies found that 41% of sera from patients with primary SS bound the 60-kd Ro peptide 21-41. Perhaps future studies will elaborate a clinical role of such a difference among SS and SLE patients. Study of the epitopes of these autoantigens has, in part, led to a new animal model of anti-Ro and anti-La. Non-autoimmune-prone animals are immunized with proteins or peptides that make up the Ro/La RNP. Such animals develop an autoimmune response to the entire particle, not just the immunogen. This response has been hypothesized to arise from autoreactive B cells. In another, older animal model of disease, the MRL-lpr/lpr mouse, B cells have recently been shown to be required for the generation of abnormal, autoreactive T cells. Thus, there are now powerful data indicating that B cells that produce autoantibodies are directly involved in the pathogenesis of disease above and beyond the formation of immune complexes. Given that the autoreactive B cell is potentially critical to the underlying pathogenesis of disease, then studying these cells will be crucial to further understanding the origin of diseases associated with Ro and La autoimmunity. Hopefully, an increased understanding will eventually lead to improved treatment of patients. Progress in the area of treatment will almost surely be incremental, and studies of the fine specificity of autoantibody binding will be a part of the body of basic knowledge contributing to ultimate advancement. In the future, the animal models will need to be examined with regard to immunology and immunochemistry as well as genetics. The development of these autoantibodies has not been studied extensively because upon presentation to medical care, virtually all patients have a full-  (+info)

Associations of anti-beta2-glycoprotein I autoantibodies with HLA class II alleles in three ethnic groups. (3/6365)

OBJECTIVE: To determine any HLA associations with anti-beta2-glycoprotein I (anti-beta2GPI) antibodies in a large, retrospectively studied, multiethnic group of 262 patients with primary antiphospholipid antibody syndrome (APS), systemic lupus erythematosus (SLE), or another connective tissue disease. METHODS: Anti-beta2GPI antibodies were detected in sera using an enzyme-linked immunosorbent assay. HLA class II alleles (DRB1, DQA1, and DQB1) were determined by DNA oligotyping. RESULTS: The HLA-DQB1*0302 (DQ8) allele, typically carried on HLA-DR4 haplotypes, was associated with anti-beta2GPI when compared with both anti-beta2GPI-negative SLE patients and ethnically matched normal controls, especially in Mexican Americans and, to a lesser extent, in whites. Similarly, when ethnic groups were combined, HLA-DQB1*0302, as well as HLA-DQB1*03 alleles overall (DQB1*0301, *0302, and *0303), were strongly correlated with anti-beta2GPI antibodies. The HLA-DR6 (DR13) haplotype DRB1*1302; DQB1*0604/5 was also significantly increased, primarily in blacks. HLA-DR7 was not significantly increased in any of these 3 ethnic groups, and HLA-DR53 (DRB4*0101) was increased in Mexican Americans only. CONCLUSION: Certain HLA class II haplotypes genetically influence the expression of antibodies to beta2GPI, an important autoimmune response in the APS, but there are variations in HLA associations among different ethnic groups.  (+info)

Estrogen enhancement of anti-double-stranded DNA antibody and immunoglobulin G production in peripheral blood mononuclear cells from patients with systemic lupus erythematosus. (4/6365)

OBJECTIVE: To study the in vitro effect of estrogen on IgG anti-double-stranded DNA (anti-dsDNA) antibody and total IgG production in peripheral blood mononuclear cells (PBMC) from patients with systemic lupus erythematosus (SLE), in order to elucidate its regulatory role in SLE. METHODS: PBMC from SLE patients and normal donors were cultured with 17beta-estradiol (E2). IgG anti-dsDNA antibodies, total IgG, and cytokine activity in the culture supernatants were measured by enzyme-linked immunosorbent assay. RESULTS: E2 enhanced production of IgG anti-dsDNA antibodies as well as total IgG in PBMC from SLE patients. Anti-dsDNA production in patients with inactive disease was less responsive to E2 than that in patients with active disease. E2 also enhanced total IgG, but not anti-dsDNA, production in the PBMC of normal donors. Antibody production was increased by E2 to a lesser extent in patients' B cells than in their PBMC. Anti-interleukin-10 (anti-IL-10) antibodies partially blocked the E2-induced increase in antibody production in patients' PBMC, but anti-IL-10 had no effect on B cells. E2 increased IL-10 production by patients' monocytes. Exogenous IL-10 acted additively with E2 in increasing antibody production in patients' B cells. CONCLUSION: These results suggest that E2 may polyclonally increase the production of IgG, including IgG anti-dsDNA, in SLE patients' PBMC by enhancing B cell activity and by promoting IL-10 production in monocytes. These findings support the involvement of E2 in the pathogenesis of SLE.  (+info)

Premature morbidity from cardiovascular and cerebrovascular diseases in women with systemic lupus erythematosus. (5/6365)

OBJECTIVE: To determine rates of morbidity due to cardiovascular and cerebrovascular diseases among women with systemic lupus erythematosus (SLE). METHODS: I used the California Hospital Discharge Database, which contains information on all discharges from acute care hospitals in California, to identify women with SLE who had been hospitalized for treatment of either acute myocardial infarction (AMI), congestive heart failure (CHF), or cerebrovascular accident (CVA) from 1991 to 1994. I compared the proportions of hospitalizations for each cause among women with SLE with those in a group of women without SLE, for 3 age strata (18-44 years, 45-64 years, and > or =65 years). RESULTS: Compared with young women without SLE, young women with SLE were 2.27 times more likely to be hospitalized because of AMI (95% confidence interval [95% CI] 1.08-3.46), 3.80 times more likely to be hospitalized because of CHF (95% CI 2.41-5.19), and 2.05 times more likely to be hospitalized because of CVA (95% CI 1.17-2.93). Among middle-aged women with SLE, the frequencies of hospitalization for AMI and CVA did not differ from those of the comparison group, but the risk of hospitalization for CHF was higher (odds ratio [OR] 1.39, 95% CI 1.05-1.73). Among elderly women with SLE, the risk of hospitalization for AMI was significantly lower (OR 0.70, 95% CI 0.51-0.89), the risk of hospitalization for CHF was higher (OR 1.25, 95% CI 1.01-1.49), and the risk of hospitalization for CVA was not significantly different from those in the comparison group. CONCLUSION: Young women with SLE are at substantially increased risk of AMI, CHF, and CVA. The relative odds of these conditions decrease with age among women with SLE.  (+info)

Unilateral cataplexy associated with systemic lupus erythematosus. (6/6365)

A patient with systemic lupus erythematosus (SLE) developed attacks of unilateral cataplexy precipitated by laughter. Unilateral cataplexy has not been described previously in detail and its association with SLE is unique. The clinical details, investigations, and diagnostic criteria are discussed and a causal relationship between cataplexy and SLE is suggested.  (+info)

Autoreactive human T cell lines recognizing ribosomal protein L7. (7/6365)

Sera of patients suffering from systemic lupus erythematosus (SLE) frequently contain oligoclonal IgG autoantibodies with high affinity for the ribosomal protein L7 (rpL7). The humoral autoimmune response to rpL7 apparently is driven by antigen and T cell dependent. In order to analyze the T cell response to rpL7 we cultured peripheral blood lymphocytes of healthy individuals and SLE patients in the presence of recombinant rpL7. After 10 days, the cytokine response to re-stimulation with rpL7 was examined using a spot-ELISA. Measuring IFN-gamma secretion, the T cells of two patients and four healthy donors showed a significant increase in the number of spots as compared to control cells. Secretion of IL-4 or IL-10 was not detected. From the antigen-stimulated primary cultures we established by limiting dilution cloning six rpL7-reactive, IFN-gamma-secreting T cell lines which show a CD3+CD4+CD8- phenotype. One line additionally was shown to be positive for HLA-DR and CD45R0, but negative for CD27 and CD31. The cell lines carry alphabeta TCR chains which differ from each other in sequence and specificity. rpL7 fragments rich in basic amino acids could be identified as epitopes recognized by the TCR of three cell lines. Recognition of rpL7 is HLA-DR6 restricted or respectively HLA-DP restricted in the two cell lines analyzed.  (+info)

Genome-wide screen for systemic lupus erythematosus susceptibility genes in multiplex families. (8/6365)

Systemic lupus erythematosus (SLE) is the prototype of human autoimmune diseases. Its genetic component has been suggested by familial aggregation (lambdas = 20) and twin studies. We have screened the human genome to localize genetic intervals that may contain lupus susceptibility loci in a sample of 188 lupus patients belonging to 80 lupus families with two or more affected relatives per family using the ABI Prism linkage mapping set which includes 350 polymorphic markers with an average spacing of 12 cM. Non-parametric multipoint linkage analysis suggests evidence for predisposing loci on chromosomes 1 and 18. However, no single locus with overwhelming evidence for linkage was found, suggesting that there are no 'major' susceptibility genes segregating in families with SLE, and that the genetic etiology is more likely to result from the action of several genes of moderate effect. Furthermore, the support for a gene in the 1q44 region as well as in the 1p36 region is clearly found only in the Mexican American families with SLE but not in families of Caucasian ethnicity, suggesting that consideration of each ethnic group separately is crucial.  (+info)

Systemic Lupus Erythematosus (SLE) is a complex autoimmune disease that can affect almost any organ or system in the body. In SLE, the immune system produces an exaggerated response, leading to the production of autoantibodies that attack the body's own cells and tissues, causing inflammation and damage. The symptoms and severity of SLE can vary widely from person to person, but common features include fatigue, joint pain, skin rashes (particularly a "butterfly" rash across the nose and cheeks), fever, hair loss, and sensitivity to sunlight.

Systemic lupus erythematosus can also affect the kidneys, heart, lungs, brain, blood vessels, and other organs, leading to a wide range of symptoms such as kidney dysfunction, chest pain, shortness of breath, seizures, and anemia. The exact cause of SLE is not fully understood, but it is believed to involve a combination of genetic, environmental, and hormonal factors. Treatment typically involves medications to suppress the immune system and manage symptoms, and may require long-term management by a team of healthcare professionals.

Discoid Lupus Erythematosus (DLE) is a chronic autoimmune disease that primarily affects the skin. It is a subtype of Cutaneous Lupus Erythematosus (CLE). DLE is characterized by coin-shaped, disc-like rashes on the face, scalp, and other sun-exposed areas of the body. These lesions are often red, scaly, and may cause scarring and pigmentation changes. Unlike Systemic Lupus Erythematosus (SLE), DLE typically does not affect internal organs, but in some cases, it can progress to SLE. The exact cause of DLE is unknown, but it is believed to be related to a combination of genetic, environmental, and hormonal factors that trigger an abnormal immune response. Treatment for DLE may include topical creams, oral medications, and avoidance of sun exposure.

Cutaneous Lupus Erythematosus (CLE) is a skin manifestation of Systemic Lupus Erythematosus (SLE), an autoimmune disease, but it can also occur without systemic involvement. It is characterized by various skin lesions that differ in appearance and distribution. The three main subtypes of CLE are:

1. Acute Cutaneous Lupus Erythematosus (ACLE): This form is typically associated with SLE and is characterized by a classic malar or "butterfly" rash on the face, which is often photosensitive and can be accompanied by discoid lesions. The rash may also appear on other sun-exposed areas of the body.

2. Chronic Cutaneous Lupus Erythematosus (CCLE): This subtype includes Discoid Lupus Erythematosus (DLE) and other less common forms such as lupus panniculitis and chilblain lupus. DLE is characterized by well-circumscribed, erythematous, scaly plaques that can cause scarring and pigmentation changes, often found on the face, scalp, and ears. Lupus panniculitis presents as deep subcutaneous nodules or indurated plaques, typically located on the trunk and proximal extremities. Chilblain lupus is characterized by violaceous, tender, and swollen lesions on acral areas, often triggered by cold exposure.

3. Subacute Cutaneous Lupus Erythematosus (SCLE): This form of CLE presents as non-scarring, papulosquamous or annular polycyclic rashes, often located on the trunk and proximal extremities. The lesions are typically photosensitive and may appear in patients with SLE or those with isolated cutaneous disease.

The diagnosis of Cutaneous Lupus Erythematosus is based on clinical presentation, histopathological findings, and sometimes direct immunofluorescence. Treatment depends on the severity and extent of skin involvement and may include topical therapies, antimalarials, corticosteroids, immunomodulatory agents, or photoprotection measures.

Lupus nephritis is a type of kidney inflammation (nephritis) that can occur in people with systemic lupus erythematosus (SLE), an autoimmune disease. In lupus nephritis, the immune system produces abnormal antibodies that attack the tissues of the kidneys, leading to inflammation and damage. The condition can cause a range of symptoms, including proteinuria (protein in the urine), hematuria (blood in the urine), hypertension (high blood pressure), and eventually kidney failure if left untreated. Lupus nephritis is typically diagnosed through a combination of medical history, physical examination, laboratory tests, and imaging studies. Treatment may include medications to suppress the immune system and control inflammation, such as corticosteroids and immunosuppressive drugs.

Antinuclear antibodies (ANA) are a type of autoantibody that target structures found in the nucleus of a cell. These antibodies are produced by the immune system and attack the body's own cells and tissues, leading to inflammation and damage. The presence of ANA is often used as a marker for certain autoimmune diseases, such as systemic lupus erythematosus (SLE), Sjogren's syndrome, rheumatoid arthritis, scleroderma, and polymyositis.

ANA can be detected through a blood test called the antinuclear antibody test. A positive result indicates the presence of ANA in the blood, but it does not necessarily mean that a person has an autoimmune disease. Further testing is usually needed to confirm a diagnosis and determine the specific type of autoantibodies present.

It's important to note that ANA can also be found in healthy individuals, particularly as they age. Therefore, the test results should be interpreted in conjunction with other clinical findings and symptoms.

Autoantibodies are defined as antibodies that are produced by the immune system and target the body's own cells, tissues, or organs. These antibodies mistakenly identify certain proteins or molecules in the body as foreign invaders and attack them, leading to an autoimmune response. Autoantibodies can be found in various autoimmune diseases such as rheumatoid arthritis, lupus, and thyroiditis. The presence of autoantibodies can also be used as a diagnostic marker for certain conditions.

Lupus vasculitis in the central nervous system (CNS) is a specific type of inflammation that occurs in the blood vessels of the brain and/or spinal cord due to systemic lupus erythematosus (SLE), an autoimmune disease. In this condition, the body's immune system mistakenly attacks healthy tissue, including blood vessel walls, leading to their inflammation and damage.

CNS vasculitis can cause various neurological symptoms such as headaches, seizures, cognitive impairment, mood changes, stroke-like episodes, and even loss of consciousness. The diagnosis typically involves a combination of clinical evaluation, imaging studies (such as MRI or angiography), and laboratory tests to detect the presence of autoantibodies associated with SLE. Treatment usually includes immunosuppressive therapy to control the inflammation and prevent further damage to the blood vessels in the CNS.

Hydroxychloroquine is an antimalarial and autoimmune disease medication. It's primarily used to prevent or treat malaria, a disease caused by parasites that enter the body through the bites of infected mosquitoes. It works by killing the malaria parasite in the red blood cells of the human body.

In addition, hydroxychloroquine is also used to treat autoimmune diseases such as rheumatoid arthritis and lupus. In these conditions, the body's immune system mistakenly attacks healthy tissues, causing inflammation and damage. Hydroxychloroquine helps to regulate the immune system and reduce inflammation.

It is important to note that while hydroxychloroquine has been studied as a potential treatment for COVID-19, current evidence does not support its use outside of a clinical trial setting due to lack of efficacy and potential for harm.

Anticardiolipin antibodies are a type of autoantibody that targets and binds to cardiolipin, a phospholipid component found in the inner mitochondrial membrane of cells. These antibodies are clinically significant because they have been associated with a variety of autoimmune disorders, including antiphospholipid syndrome (APS).

APS is a condition characterized by recurrent blood clots, pregnancy losses, and thrombocytopenia (low platelet count). Anticardiolipin antibodies are one of the three main types of autoantibodies found in APS, along with lupus anticoagulant and anti-β2 glycoprotein I antibodies.

The presence of high levels of anticardiolipin antibodies in the blood can lead to abnormal blood clotting, which can cause serious complications such as deep vein thrombosis, pulmonary embolism, and stroke. Anticardiolipin antibodies can also contribute to pregnancy losses by causing placental insufficiency or abnormal blood clotting in the placenta.

Anticardiolipin antibodies are typically detected through a blood test that measures their levels in the serum. A positive result is usually confirmed with a second test performed at least 12 weeks later to establish persistence. Treatment for anticardiolipin antibody-related disorders typically involves anticoagulation therapy to prevent blood clots and other complications.

'NZB mice' is a term used to refer to an inbred strain of laboratory mice that are genetically identical to each other and have been used extensively in biomedical research. The 'NZB' designation stands for "New Zealand Black," which refers to the coat color of these mice.

NZB mice are known to spontaneously develop an autoimmune disease that is similar to human systemic lupus erythematosus (SLE), a chronic inflammatory disorder caused by an overactive immune system. This makes them a valuable model for studying the genetic and environmental factors that contribute to the development of SLE, as well as for testing new therapies and treatments.

It's important to note that while NZB mice are an inbred strain, they may still exhibit some variability in their disease phenotype due to genetic modifiers or environmental influences. Therefore, researchers often use large cohorts of mice and standardized experimental conditions to ensure the reproducibility and reliability of their findings.

Antiphospholipid antibodies are a type of autoantibody that targets and binds to certain proteins found in the blood that attach to phospholipids (a type of fat molecule). These antibodies are associated with an increased risk of developing antiphospholipid syndrome, a disorder characterized by abnormal blood clotting.

There are several types of antiphospholipid antibodies, including:

1. Lupus anticoagulant: This type of antiphospholipid antibody can interfere with blood clotting tests and may increase the risk of thrombosis (blood clots) in both arteries and veins.
2. Anticardiolipin antibodies: These antibodies target a specific phospholipid called cardiolipin, which is found in the inner membrane of mitochondria. High levels of anticardiolipin antibodies are associated with an increased risk of thrombosis and pregnancy complications such as recurrent miscarriage.
3. Anti-β2 glycoprotein I antibodies: These antibodies target a protein called β2 glycoprotein I, which binds to negatively charged phospholipids on the surface of cells. High levels of anti-β2 glycoprotein I antibodies are associated with an increased risk of thrombosis and pregnancy complications.

The exact mechanism by which antiphospholipid antibodies cause blood clotting is not fully understood, but it is thought to involve the activation of platelets, the inhibition of natural anticoagulants, and the promotion of inflammation. Antiphospholipid syndrome can be treated with medications that thin the blood or prevent clots from forming, such as aspirin, warfarin, or heparin.

Autoantigens are substances that are typically found in an individual's own body, but can stimulate an immune response because they are recognized as foreign by the body's own immune system. In autoimmune diseases, the immune system mistakenly attacks and damages healthy tissues and organs because it recognizes some of their components as autoantigens. These autoantigens can be proteins, DNA, or other molecules that are normally present in the body but have become altered or exposed due to various factors such as infection, genetics, or environmental triggers. The immune system then produces antibodies and activates immune cells to attack these autoantigens, leading to tissue damage and inflammation.

Antiphospholipid syndrome (APS) is an autoimmune disorder characterized by the presence of antiphospholipid antibodies in the blood. These antibodies are directed against phospholipids, a type of fat molecule found in cell membranes and plasma lipoproteins. The presence of these antibodies can lead to abnormal blood clotting, which can cause serious complications such as stroke, heart attack, deep vein thrombosis, and pulmonary embolism.

APS can occur either on its own (primary APS) or in conjunction with other autoimmune disorders, such as systemic lupus erythematosus (secondary APS). The exact cause of APS is not fully understood, but it is believed to involve a combination of genetic and environmental factors.

Symptoms of APS can vary widely depending on the location and severity of the blood clots. They may include:

* Recurrent miscarriages or stillbirths
* Blood clots in the legs, lungs, or other parts of the body
* Skin ulcers or lesions
* Headaches, seizures, or stroke-like symptoms
* Kidney problems
* Heart valve abnormalities

Diagnosis of APS typically involves blood tests to detect the presence of antiphospholipid antibodies. Treatment may include medications to prevent blood clots, such as anticoagulants and antiplatelet agents, as well as management of any underlying autoimmune disorders.

Autoimmune diseases are a group of disorders in which the immune system, which normally protects the body from foreign invaders like bacteria and viruses, mistakenly attacks the body's own cells and tissues. This results in inflammation and damage to various organs and tissues in the body.

In autoimmune diseases, the body produces autoantibodies that target its own proteins or cell receptors, leading to their destruction or malfunction. The exact cause of autoimmune diseases is not fully understood, but it is believed that a combination of genetic and environmental factors contribute to their development.

There are over 80 different types of autoimmune diseases, including rheumatoid arthritis, lupus, multiple sclerosis, type 1 diabetes, Hashimoto's thyroiditis, Graves' disease, psoriasis, and inflammatory bowel disease. Symptoms can vary widely depending on the specific autoimmune disease and the organs or tissues affected. Treatment typically involves managing symptoms and suppressing the immune system to prevent further damage.

Immunoglobulin G (IgG) is a type of antibody, which is a protective protein produced by the immune system in response to foreign substances like bacteria or viruses. IgG is the most abundant type of antibody in human blood, making up about 75-80% of all antibodies. It is found in all body fluids and plays a crucial role in fighting infections caused by bacteria, viruses, and toxins.

IgG has several important functions:

1. Neutralization: IgG can bind to the surface of bacteria or viruses, preventing them from attaching to and infecting human cells.
2. Opsonization: IgG coats the surface of pathogens, making them more recognizable and easier for immune cells like neutrophils and macrophages to phagocytose (engulf and destroy) them.
3. Complement activation: IgG can activate the complement system, a group of proteins that work together to help eliminate pathogens from the body. Activation of the complement system leads to the formation of the membrane attack complex, which creates holes in the cell membranes of bacteria, leading to their lysis (destruction).
4. Antibody-dependent cellular cytotoxicity (ADCC): IgG can bind to immune cells like natural killer (NK) cells and trigger them to release substances that cause target cells (such as virus-infected or cancerous cells) to undergo apoptosis (programmed cell death).
5. Immune complex formation: IgG can form immune complexes with antigens, which can then be removed from the body through various mechanisms, such as phagocytosis by immune cells or excretion in urine.

IgG is a critical component of adaptive immunity and provides long-lasting protection against reinfection with many pathogens. It has four subclasses (IgG1, IgG2, IgG3, and IgG4) that differ in their structure, function, and distribution in the body.

'Mice, Inbred MRL-lpr' refers to a specific strain of laboratory mice that are used in biomedical research. The 'MRL' part of the name stands for the breeding colony where they were originally developed, which is the Mouse Repository at the Jackson Laboratory in Bar Harbor, Maine. The 'lpr' designation indicates that these mice carry a mutation in the Fas gene, also known as lpr (lymphoproliferation) gene, which leads to an autoimmune disorder characterized by lymphadenopathy (enlarged lymph nodes), splenomegaly (enlarged spleen), and production of autoantibodies.

The MRL-lpr mice are known for their accelerated aging phenotype, which includes the development of a variety of age-related diseases such as atherosclerosis, osteoporosis, and cancer. They also develop a severe form of systemic lupus erythematosus (SLE), an autoimmune disease that affects many organs in the body. The MRL-lpr mice are widely used as a model to study the pathogenesis of SLE and other autoimmune diseases, as well as to test potential therapies for these conditions.

It is important to note that while inbred mouse strains like MRL-lpr provide valuable insights into human disease mechanisms, they do not perfectly replicate all aspects of human disease, and results obtained in mice may not always translate directly to humans. Therefore, findings from mouse studies should be interpreted with caution and validated in human studies before being applied in clinical practice.

Complement C4 is a protein that plays a crucial role in the complement system, which is a part of the immune system that helps to clear pathogens and damaged cells from the body. Complement C4 is involved in the early stages of the complement activation cascade, where it helps to identify and tag foreign or abnormal cells for destruction by other components of the immune system.

Specifically, Complement C4 can be cleaved into two smaller proteins, C4a and C4b, during the complement activation process. C4b then binds to the surface of the target cell and helps to initiate the formation of the membrane attack complex (MAC), which creates a pore in the cell membrane and leads to lysis or destruction of the target cell.

Deficiencies or mutations in the Complement C4 gene can lead to various immune disorders, including certain forms of autoimmune diseases and susceptibility to certain infections.

I'm sorry for any confusion, but "Lupus Coagulation Inhibitor" is not a recognized medical term or concept in hematology or immunology.

Systemic Lupus Erythematosus (SLE), often referred to simply as lupus, is an autoimmune disease where the body's immune system mistakenly attacks healthy tissue. However, this does not result in a specific coagulation inhibitor.

If you're asking about lupus anticoagulants, these are antibodies that can interfere with clotting tests but paradoxically increase the risk of blood clots in vivo. They are sometimes seen in patients with SLE and other autoimmune diseases.

Please provide more context if you meant something else, so I can give a more accurate response.

SnRNP (small nuclear ribonucleoprotein) core proteins are a group of proteins that are associated with small nuclear RNAs (snRNAs) to form small nuclear ribonucleoprotein particles. These particles play crucial roles in various aspects of RNA processing, such as splicing, 3' end formation, and degradation.

The snRNP core proteins include seven Sm proteins (B, D1, D2, D3, E, F, and G) that form a heptameric ring-like structure called the Sm core, which binds to a conserved sequence motif in the snRNAs called the Sm site. In addition to the Sm proteins, there are also other core proteins such as Sm like (L) proteins and various other protein factors that associate with specific snRNP particles.

Together, these snRNP core proteins help to stabilize the snRNA, facilitate its assembly into functional ribonucleoprotein complexes, and participate in the recognition and processing of target RNAs during post-transcriptional regulation.

An antigen-antibody complex is a type of immune complex that forms when an antibody binds to a specific antigen. An antigen is any substance that triggers an immune response, while an antibody is a protein produced by the immune system to neutralize or destroy foreign substances like antigens.

When an antibody binds to an antigen, it forms a complex that can be either soluble or insoluble. Soluble complexes are formed when the antigen is small and can move freely through the bloodstream. Insoluble complexes, on the other hand, are formed when the antigen is too large to move freely, such as when it is part of a bacterium or virus.

The formation of antigen-antibody complexes plays an important role in the immune response. Once formed, these complexes can be recognized and cleared by other components of the immune system, such as phagocytes, which help to prevent further damage to the body. However, in some cases, the formation of large numbers of antigen-antibody complexes can lead to inflammation and tissue damage, contributing to the development of certain autoimmune diseases.

Lupus erythematosus panniculitis (LEP), also known as lupus profundus, is a type of cutaneous lupus erythematosus (CLE) that affects the fatty layer under the skin (subcutaneous tissue). It is characterized by deep inflammation of the fatty tissue, leading to nodular or indurated (hardened) plaques and subcutaneous ulcerations. The lesions are typically tender and can be painful. LEP most commonly affects the face, trunk, and proximal extremities.

LEP is associated with systemic lupus erythematosus (SLE), but it can also occur in isolation without evidence of systemic involvement. It is estimated that approximately 1-10% of patients with SLE develop LEP. The exact pathogenesis of LEP remains unclear, but it is thought to involve an autoimmune response directed against the fatty tissue.

Histologically, LEP is characterized by lobular panniculitis with lymphocytic infiltration and fat necrosis. Direct immunofluorescence may show deposition of immune complexes along the blood vessels in the affected area.

Treatment of LEP can be challenging, and often requires a multidisciplinary approach involving dermatologists, rheumatologists, and other specialists. Systemic therapies such as corticosteroids, antimalarials, immunosuppressive agents, and biologics may be used to control the disease activity. In addition, local treatments such as intralesional steroid injections or surgical excision of lesions may be considered for refractory cases.

Rheumatic diseases are a group of disorders that cause pain, stiffness, and swelling in the joints, muscles, tendons, ligaments, or bones. They include conditions such as rheumatoid arthritis, osteoarthritis, systemic lupus erythematosus (SLE), gout, ankylosing spondylitis, psoriatic arthritis, and many others. These diseases can also affect other body systems including the skin, eyes, lungs, heart, kidneys, and nervous system. Rheumatic diseases are often chronic and may be progressive, meaning they can worsen over time. They can cause significant pain, disability, and reduced quality of life if not properly diagnosed and managed. The exact causes of rheumatic diseases are not fully understood, but genetics, environmental factors, and immune system dysfunction are believed to play a role in their development.

Autoimmunity is a medical condition in which the body's immune system mistakenly attacks and destroys healthy tissues within the body. In normal function, the immune system recognizes and fights off foreign substances such as bacteria, viruses, and toxins. However, when autoimmunity occurs, the immune system identifies self-molecules or tissues as foreign and produces an immune response against them.

This misguided response can lead to chronic inflammation, tissue damage, and impaired organ function. Autoimmune diseases can affect various parts of the body, including the joints, skin, glands, muscles, and blood vessels. Some common examples of autoimmune diseases are rheumatoid arthritis, lupus, multiple sclerosis, type 1 diabetes, Hashimoto's thyroiditis, and Graves' disease.

The exact cause of autoimmunity is not fully understood, but it is believed to involve a combination of genetic, environmental, and lifestyle factors that trigger an abnormal immune response in susceptible individuals. Treatment for autoimmune diseases typically involves managing symptoms, reducing inflammation, and suppressing the immune system's overactive response using medications such as corticosteroids, immunosuppressants, and biologics.

Rheumatoid arthritis (RA) is a systemic autoimmune disease that primarily affects the joints. It is characterized by persistent inflammation, synovial hyperplasia, and subsequent damage to the articular cartilage and bone. The immune system mistakenly attacks the body's own tissues, specifically targeting the synovial membrane lining the joint capsule. This results in swelling, pain, warmth, and stiffness in affected joints, often most severely in the hands and feet.

RA can also have extra-articular manifestations, affecting other organs such as the lungs, heart, skin, eyes, and blood vessels. The exact cause of RA remains unknown, but it is believed to involve a complex interplay between genetic susceptibility and environmental triggers. Early diagnosis and treatment are crucial in managing rheumatoid arthritis to prevent joint damage, disability, and systemic complications.

Sjögren's syndrome is a chronic autoimmune disorder in which the body's immune system mistakenly attacks its own moisture-producing glands, particularly the tear and salivary glands. This can lead to symptoms such as dry eyes, dry mouth, and dryness in other areas of the body. In some cases, it may also affect other organs, leading to a variety of complications.

There are two types of Sjögren's syndrome: primary and secondary. Primary Sjögren's syndrome occurs when the condition develops on its own, while secondary Sjögren's syndrome occurs when it develops in conjunction with another autoimmune disease, such as rheumatoid arthritis or lupus.

The exact cause of Sjögren's syndrome is not fully understood, but it is believed to involve a combination of genetic and environmental factors. Treatment typically focuses on relieving symptoms and may include artificial tears, saliva substitutes, medications to stimulate saliva production, and immunosuppressive drugs in more severe cases.

Complement C1q is a protein that is part of the complement system, which is a group of proteins in the blood that help to eliminate pathogens and damaged cells from the body. C1q is the first component of the classical complement pathway, which is activated by the binding of C1q to antibodies that are attached to the surface of a pathogen or damaged cell.

C1q is composed of six identical polypeptide chains, each containing a collagen-like region and a globular head region. The globular heads can bind to various structures, including the Fc regions of certain antibodies, immune complexes, and some types of cells. When C1q binds to an activating surface, it triggers a series of proteolytic reactions that lead to the activation of other complement components and the formation of the membrane attack complex (MAC), which can punch holes in the membranes of pathogens or damaged cells, leading to their destruction.

In addition to its role in the immune system, C1q has also been found to have roles in various physiological processes, including tissue remodeling, angiogenesis, and the clearance of apoptotic cells. Dysregulation of the complement system, including abnormalities in C1q function, has been implicated in a variety of diseases, including autoimmune disorders, inflammatory diseases, and neurodegenerative conditions.

Nephritis is a medical term that refers to inflammation of the kidneys, specifically affecting the glomeruli - the tiny filtering units inside the kidneys. The condition can cause damage to the glomeruli, leading to impaired kidney function and the leakage of protein and blood into the urine.

Nephritis can result from a variety of causes, including infections, autoimmune disorders, and exposure to certain medications or toxins. Depending on the severity and underlying cause, nephritis may be treated with medications, dietary modifications, or other therapies aimed at reducing inflammation and preserving kidney function. In severe cases, hospitalization and more intensive treatments may be necessary.

Photosensitivity disorders refer to conditions that cause an abnormal reaction to sunlight or artificial light. This reaction can take the form of various skin changes, such as rashes, inflammation, or pigmentation, and in some cases, it can also lead to systemic symptoms like fatigue, fever, or joint pain.

The two main types of photosensitivity disorders are:

1. Phototoxic reactions: These occur when a substance (such as certain medications, chemicals, or plants) absorbs light energy and transfers it to skin cells, causing damage and inflammation. The reaction typically appears within 24 hours of exposure to the light source and can resemble a sunburn.

2. Photoallergic reactions: These occur when the immune system responds to the combination of light and a particular substance, leading to an allergic response. The reaction may not appear until several days after initial exposure and can cause redness, itching, and blistering.

It is important for individuals with photosensitivity disorders to avoid excessive sun exposure, wear protective clothing, and use broad-spectrum sunscreens with a high SPF rating to minimize the risk of phototoxic or photoallergic reactions.

A Severity of Illness Index is a measurement tool used in healthcare to assess the severity of a patient's condition and the risk of mortality or other adverse outcomes. These indices typically take into account various physiological and clinical variables, such as vital signs, laboratory values, and co-morbidities, to generate a score that reflects the patient's overall illness severity.

Examples of Severity of Illness Indices include the Acute Physiology and Chronic Health Evaluation (APACHE) system, the Simplified Acute Physiology Score (SAPS), and the Mortality Probability Model (MPM). These indices are often used in critical care settings to guide clinical decision-making, inform prognosis, and compare outcomes across different patient populations.

It is important to note that while these indices can provide valuable information about a patient's condition, they should not be used as the sole basis for clinical decision-making. Rather, they should be considered in conjunction with other factors, such as the patient's overall clinical presentation, treatment preferences, and goals of care.

Prednisolone is a synthetic glucocorticoid drug, which is a class of steroid hormones. It is commonly used in the treatment of various inflammatory and autoimmune conditions due to its potent anti-inflammatory and immunosuppressive effects. Prednisolone works by binding to specific receptors in cells, leading to changes in gene expression that reduce the production of substances involved in inflammation, such as cytokines and prostaglandins.

Prednisolone is available in various forms, including tablets, syrups, and injectable solutions. It can be used to treat a wide range of medical conditions, including asthma, rheumatoid arthritis, inflammatory bowel disease, allergies, skin conditions, and certain types of cancer.

Like other steroid medications, prednisolone can have significant side effects if used in high doses or for long periods of time. These may include weight gain, mood changes, increased risk of infections, osteoporosis, diabetes, and adrenal suppression. As a result, the use of prednisolone should be closely monitored by a healthcare professional to ensure that its benefits outweigh its risks.

Complement C3 is a protein that plays a central role in the complement system, which is a part of the immune system that helps to clear pathogens and damaged cells from the body. Complement C3 can be activated through three different pathways: the classical pathway, the lectin pathway, and the alternative pathway. Once activated, it breaks down into two fragments, C3a and C3b.

C3a is an anaphylatoxin that helps to recruit immune cells to the site of infection or injury, while C3b plays a role in opsonization, which is the process of coating pathogens or damaged cells with proteins to make them more recognizable to the immune system. Additionally, C3b can also activate the membrane attack complex (MAC), which forms a pore in the membrane of target cells leading to their lysis or destruction.

In summary, Complement C3 is an important protein in the complement system that helps to identify and eliminate pathogens and damaged cells from the body through various mechanisms.

"Small cytoplasmic RNAs" (scRNAs) are a heterogeneous group of non-coding RNA molecules that are typically 100-300 nucleotides in length and are located within the cytoplasm of cells. They play various roles in post-transcriptional regulation of gene expression, including serving as components of ribonucleoprotein complexes involved in mRNA splicing, stability, and translation.

Some specific types of scRNAs include small nuclear RNAs (snRNAs), which are involved in spliceosomal complexes that remove introns from pre-mRNA; small nucleolar RNAs (snoRNAs), which guide chemical modifications of other RNA molecules, such as ribosomal RNAs (rRNAs); and microRNAs (miRNAs), which bind to target mRNAs and inhibit their translation or promote their degradation.

It's worth noting that the term "small cytoplasmic RNA" is a broad category, and individual scRNAs can have distinct functions and characteristics.

B-lymphocytes, also known as B-cells, are a type of white blood cell that plays a key role in the immune system's response to infection. They are responsible for producing antibodies, which are proteins that help to neutralize or destroy pathogens such as bacteria and viruses.

When a B-lymphocyte encounters a pathogen, it becomes activated and begins to divide and differentiate into plasma cells, which produce and secrete large amounts of antibodies specific to the antigens on the surface of the pathogen. These antibodies bind to the pathogen, marking it for destruction by other immune cells such as neutrophils and macrophages.

B-lymphocytes also have a role in presenting antigens to T-lymphocytes, another type of white blood cell involved in the immune response. This helps to stimulate the activation and proliferation of T-lymphocytes, which can then go on to destroy infected cells or help to coordinate the overall immune response.

Overall, B-lymphocytes are an essential part of the adaptive immune system, providing long-lasting immunity to previously encountered pathogens and helping to protect against future infections.

Deoxyribonucleic acid (DNA) is the genetic material present in the cells of organisms where it is responsible for the storage and transmission of hereditary information. DNA is a long molecule that consists of two strands coiled together to form a double helix. Each strand is made up of a series of four nucleotide bases - adenine (A), guanine (G), cytosine (C), and thymine (T) - that are linked together by phosphate and sugar groups. The sequence of these bases along the length of the molecule encodes genetic information, with A always pairing with T and C always pairing with G. This base-pairing allows for the replication and transcription of DNA, which are essential processes in the functioning and reproduction of all living organisms.

Immunosuppressive agents are medications that decrease the activity of the immune system. They are often used to prevent the rejection of transplanted organs and to treat autoimmune diseases, where the immune system mistakenly attacks the body's own tissues. These drugs work by interfering with the immune system's normal responses, which helps to reduce inflammation and damage to tissues. However, because they suppress the immune system, people who take immunosuppressive agents are at increased risk for infections and other complications. Examples of immunosuppressive agents include corticosteroids, azathioprine, cyclophosphamide, mycophenolate mofetil, tacrolimus, and sirolimus.

Connective tissue diseases (CTDs) are a group of disorders that involve the abnormal production and accumulation of abnormal connective tissues in various parts of the body. Connective tissues are the structural materials that support and bind other tissues and organs together. They include tendons, ligaments, cartilage, fat, and the material that fills the spaces between cells, called the extracellular matrix.

Connective tissue diseases can affect many different systems in the body, including the skin, joints, muscles, lungs, kidneys, gastrointestinal tract, and blood vessels. Some CTDs are autoimmune disorders, meaning that the immune system mistakenly attacks healthy connective tissues. Others may be caused by genetic mutations or environmental factors.

Some examples of connective tissue diseases include:

* Systemic lupus erythematosus (SLE)
* Rheumatoid arthritis (RA)
* Scleroderma
* Dermatomyositis/Polymyositis
* Mixed Connective Tissue Disease (MCTD)
* Sjogren's syndrome
* Ehlers-Danlos syndrome
* Marfan syndrome
* Osteogenesis imperfecta

The specific symptoms and treatment of connective tissue diseases vary depending on the type and severity of the condition. Treatment may include medications to reduce inflammation, suppress the immune system, or manage pain. In some cases, surgery may be necessary to repair or replace damaged tissues or organs.

Immunoglobulin M (IgM) is a type of antibody that is primarily found in the blood and lymph fluid. It is the first antibody to be produced in response to an initial exposure to an antigen, making it an important part of the body's primary immune response. IgM antibodies are large molecules that are composed of five basic units, giving them a pentameric structure. They are primarily found on the surface of B cells as membrane-bound immunoglobulins (mlgM), where they function as receptors for antigens. Once an mlgM receptor binds to an antigen, it triggers the activation and differentiation of the B cell into a plasma cell that produces and secretes large amounts of soluble IgM antibodies.

IgM antibodies are particularly effective at agglutination (clumping) and complement activation, which makes them important in the early stages of an immune response to help clear pathogens from the bloodstream. However, they are not as stable or long-lived as other types of antibodies, such as IgG, and their levels tend to decline after the initial immune response has occurred.

In summary, Immunoglobulin M (IgM) is a type of antibody that plays a crucial role in the primary immune response to antigens by agglutination and complement activation. It is primarily found in the blood and lymph fluid, and it is produced by B cells after they are activated by an antigen.

A case-control study is an observational research design used to identify risk factors or causes of a disease or health outcome. In this type of study, individuals with the disease or condition (cases) are compared with similar individuals who do not have the disease or condition (controls). The exposure history or other characteristics of interest are then compared between the two groups to determine if there is an association between the exposure and the disease.

Case-control studies are often used when it is not feasible or ethical to conduct a randomized controlled trial, as they can provide valuable insights into potential causes of diseases or health outcomes in a relatively short period of time and at a lower cost than other study designs. However, because case-control studies rely on retrospective data collection, they are subject to biases such as recall bias and selection bias, which can affect the validity of the results. Therefore, it is important to carefully design and conduct case-control studies to minimize these potential sources of bias.

An Enzyme-Linked Immunosorbent Assay (ELISA) is a type of analytical biochemistry assay used to detect and quantify the presence of a substance, typically a protein or peptide, in a liquid sample. It takes its name from the enzyme-linked antibodies used in the assay.

In an ELISA, the sample is added to a well containing a surface that has been treated to capture the target substance. If the target substance is present in the sample, it will bind to the surface. Next, an enzyme-linked antibody specific to the target substance is added. This antibody will bind to the captured target substance if it is present. After washing away any unbound material, a substrate for the enzyme is added. If the enzyme is present due to its linkage to the antibody, it will catalyze a reaction that produces a detectable signal, such as a color change or fluorescence. The intensity of this signal is proportional to the amount of target substance present in the sample, allowing for quantification.

ELISAs are widely used in research and clinical settings to detect and measure various substances, including hormones, viruses, and bacteria. They offer high sensitivity, specificity, and reproducibility, making them a reliable choice for many applications.

Genetic predisposition to disease refers to an increased susceptibility or vulnerability to develop a particular illness or condition due to inheriting specific genetic variations or mutations from one's parents. These genetic factors can make it more likely for an individual to develop a certain disease, but it does not guarantee that the person will definitely get the disease. Environmental factors, lifestyle choices, and interactions between genes also play crucial roles in determining if a genetically predisposed person will actually develop the disease. It is essential to understand that having a genetic predisposition only implies a higher risk, not an inevitable outcome.

B-cell activating factor (BAFF) is a type of protein belonging to the tumor necrosis factor (TNF) family. Its primary function is to stimulate and activate B cells, which are a type of white blood cell that plays a crucial role in the immune system by producing antibodies. BAFF helps to promote the survival, differentiation, and activation of B cells, thereby contributing to the adaptive immune response.

BAFF binds to its receptor, known as BAFF receptor (BAFF-R), which is expressed on the surface of B cells. This interaction leads to the activation of various signaling pathways that promote B cell survival and proliferation. Overexpression or excessive production of BAFF has been implicated in several autoimmune diseases, such as rheumatoid arthritis, systemic lupus erythematosus (SLE), and Sjogren's syndrome, due to the abnormal activation and expansion of B cells.

In summary, B-cell activating factor is a protein that plays an essential role in the activation and survival of B cells, which are crucial for the immune response. However, its overexpression or dysregulation can contribute to the development of autoimmune diseases.

Cardiolipins are a type of phospholipid that are primarily found in the inner mitochondrial membrane of cells. They play a crucial role in several important cellular processes, including energy production, apoptosis (programmed cell death), and maintenance of the structural integrity of the mitochondria.

Cardiolipins are unique because they contain four fatty acid chains, whereas most other phospholipids contain only two. This gives cardiolipins a distinctive conical shape that is important for their function in maintaining the curvature and stability of the inner mitochondrial membrane.

Cardiolipins have also been implicated in various diseases, including neurodegenerative disorders, cancer, and bacterial infections. For example, changes in cardiolipin composition or distribution have been linked to mitochondrial dysfunction in Parkinson's disease and other neurological conditions. Additionally, certain bacteria, such as Neisseria gonorrhoeae and Chlamydia trachomatis, can manipulate host cell cardiolipins to facilitate their own survival and replication.

In summary, cardiolipins are essential phospholipids found in the inner mitochondrial membrane that play a critical role in several cellular processes, and have been implicated in various diseases.

Collagen diseases, also known as collagen disorders or connective tissue diseases, refer to a group of medical conditions that affect the body's connective tissues. These tissues provide support and structure for various organs and systems in the body, including the skin, joints, muscles, and blood vessels.

Collagen is a major component of connective tissues, and it plays a crucial role in maintaining their strength and elasticity. In collagen diseases, the body's immune system mistakenly attacks healthy collagen, leading to inflammation, pain, and damage to the affected tissues.

There are several types of collagen diseases, including:

1. Systemic Lupus Erythematosus (SLE): This is a chronic autoimmune disease that can affect various organs and systems in the body, including the skin, joints, kidneys, heart, and lungs.
2. Rheumatoid Arthritis (RA): This is a chronic inflammatory disease that primarily affects the joints, causing pain, swelling, and stiffness.
3. Scleroderma: This is a rare autoimmune disorder that causes thickening and hardening of the skin and connective tissues, leading to restricted movement and organ damage.
4. Dermatomyositis: This is an inflammatory muscle disease that can also affect the skin, causing rashes and weakness.
5. Mixed Connective Tissue Disease (MCTD): This is a rare autoimmune disorder that combines symptoms of several collagen diseases, including SLE, RA, scleroderma, and dermatomyositis.

The exact cause of collagen diseases is not fully understood, but they are believed to be related to genetic, environmental, and hormonal factors. Treatment typically involves a combination of medications, lifestyle changes, and physical therapy to manage symptoms and prevent complications.

Mixed Connective Tissue Disease (MCTD) is a rare overlapping condition of the connective tissues, characterized by the presence of specific autoantibodies against a protein called "U1-snRNP" or "U1-small nuclear ribonucleoprotein." This disorder has features of various connective tissue diseases such as systemic lupus erythematosus (SLE), scleroderma, polymyositis, and rheumatoid arthritis. Symptoms may include swollen hands, joint pain and swelling, muscle weakness, skin thickening, lung involvement, and Raynaud's phenomenon. The exact cause of MCTD is unknown, but it is believed to involve both genetic and environmental factors leading to an autoimmune response. Early diagnosis and treatment are essential for better disease management and preventing severe complications.

Complement C4a is a protein fragment or cleavage product generated during the activation of the complement system, which is a part of the immune system. The complement system helps to eliminate pathogens and damaged cells by marking them for destruction and direct lysis. Complement component 4 (C4) is one of the key proteins in this cascade, and it gets cleaved into C4a and C4b during the activation process.

C4a is a small anaphylatoxin with a molecular weight of approximately 9 kDa. It has chemotactic properties, meaning it can attract immune cells like neutrophils to the site of complement activation. Additionally, C4a can induce histamine release from mast cells and basophils, contributing to local inflammation. However, its precise physiological role in the immune response is not entirely clear, and dysregulation of C4a production has been implicated in several pathological conditions, such as autoimmune diseases and allergies.

Serositis is a medical term that refers to inflammation of the serous membranes, which are thin layers of tissue that line the inner surfaces of body cavities and surround organs such as the heart, lungs, and abdomen. The serous membranes produce a lubricating fluid called serous fluid that helps reduce friction between internal organs and enables them to move smoothly against each other.

Inflammation of these membranes can result in excessive production of serous fluid, leading to the accumulation of fluid in the surrounding body cavities. This accumulation can cause symptoms such as chest pain, coughing, difficulty breathing, or abdominal swelling and discomfort.

Serositis is often associated with various medical conditions, including autoimmune diseases like rheumatoid arthritis, lupus, and Sjogren's syndrome. Infections, cancers, and certain medications may also cause serositis. Treatment typically involves addressing the underlying condition causing the inflammation and managing symptoms with medications such as nonsteroidal anti-inflammatory drugs (NSAIDs), corticosteroids, or immunosuppressive agents.

Systemic Scleroderma, also known as Systemic Sclerosis (SSc), is a rare, chronic autoimmune disease that involves the abnormal growth and accumulation of collagen in various connective tissues, blood vessels, and organs throughout the body. This excessive collagen production leads to fibrosis or scarring, which can cause thickening, hardening, and tightening of the skin and damage to internal organs such as the heart, lungs, kidneys, and gastrointestinal tract.

Systemic Scleroderma is characterized by two main features: small blood vessel abnormalities (Raynaud's phenomenon) and fibrosis. The disease can be further classified into two subsets based on the extent of skin involvement: limited cutaneous systemic sclerosis (lcSSc) and diffuse cutaneous systemic sclerosis (dcSSc).

Limited cutaneous systemic sclerosis affects the skin distally, typically involving fingers, hands, forearms, feet, lower legs, and face. It is often associated with Raynaud's phenomenon, calcinosis, telangiectasias, and pulmonary arterial hypertension.

Diffuse cutaneous systemic sclerosis involves more extensive skin thickening and fibrosis that spreads proximally to affect the trunk, upper arms, thighs, and face. It is commonly associated with internal organ involvement, such as interstitial lung disease, heart disease, and kidney problems.

The exact cause of Systemic Scleroderma remains unknown; however, it is believed that genetic, environmental, and immunological factors contribute to its development. There is currently no cure for Systemic Scleroderma, but various treatments can help manage symptoms, slow disease progression, and improve quality of life.

Lupus vulgaris is not related to systemic lupus erythematosus, which is an autoimmune disease. Instead, it's a specific form of cutaneous tuberculosis, a bacterial infection that affects the skin. It's caused by the Mycobacterium tuberculosis bacteria, the same organism responsible for pulmonary tuberculosis and other forms of tuberculosis.

Lupus vulgaris typically occurs in people who have had prior tuberculous infection or those with a weakened immune system. The condition is characterized by slowly growing, reddish-brown or violaceous papules, nodules, and plaques that may ulcerate and form scars. Lesions often have an apple jelly appearance when a glass slide is pressed against them and examined under a dermatoscope.

Lupus vulgaris lesions usually occur on the face, especially the nose, cheeks, and ears, but they can appear on other parts of the body as well. The condition can lead to significant disfigurement if left untreated. Diagnosis typically involves skin biopsy and culture or PCR for Mycobacterium tuberculosis. Treatment usually consists of a combination of multiple antituberculous drugs, such as isoniazid, rifampin, ethambutol, and pyrazinamide, along with local therapies like surgical excision or laser treatment.

Glomerulonephritis is a medical condition that involves inflammation of the glomeruli, which are the tiny blood vessel clusters in the kidneys that filter waste and excess fluids from the blood. This inflammation can impair the kidney's ability to filter blood properly, leading to symptoms such as proteinuria (protein in the urine), hematuria (blood in the urine), edema (swelling), hypertension (high blood pressure), and eventually kidney failure.

Glomerulonephritis can be acute or chronic, and it may occur as a primary kidney disease or secondary to other medical conditions such as infections, autoimmune disorders, or vasculitis. The diagnosis of glomerulonephritis typically involves a combination of medical history, physical examination, urinalysis, blood tests, and imaging studies, with confirmation often requiring a kidney biopsy. Treatment depends on the underlying cause and severity of the disease but may include medications to suppress inflammation, control blood pressure, and manage symptoms.

Ribonucleoproteins (RNPs) are complexes composed of ribonucleic acid (RNA) and proteins. They play crucial roles in various cellular processes, including gene expression, RNA processing, transport, stability, and degradation. Different types of RNPs exist, such as ribosomes, spliceosomes, and signal recognition particles, each having specific functions in the cell.

Ribosomes are large RNP complexes responsible for protein synthesis, where messenger RNA (mRNA) is translated into proteins. They consist of two subunits: a smaller subunit containing ribosomal RNA (rRNA) and proteins that recognize the start codon on mRNA, and a larger subunit with rRNA and proteins that facilitate peptide bond formation during translation.

Spliceosomes are dynamic RNP complexes involved in pre-messenger RNA (pre-mRNA) splicing, where introns (non-coding sequences) are removed, and exons (coding sequences) are joined together to form mature mRNA. Spliceosomes consist of five small nuclear ribonucleoproteins (snRNPs), each containing a specific small nuclear RNA (snRNA) and several proteins, as well as numerous additional proteins.

Other RNP complexes include signal recognition particles (SRPs), which are responsible for targeting secretory and membrane proteins to the endoplasmic reticulum during translation, and telomerase, an enzyme that maintains the length of telomeres (the protective ends of chromosomes) by adding repetitive DNA sequences using its built-in RNA component.

In summary, ribonucleoproteins are essential complexes in the cell that participate in various aspects of RNA metabolism and protein synthesis.

Small nuclear ribonucleoproteins (snRNPs) are a type of ribonucleoprotein (RNP) found within the nucleus of eukaryotic cells. They are composed of small nuclear RNA (snRNA) molecules and associated proteins, which are involved in various aspects of RNA processing, particularly in the modification and splicing of messenger RNA (mRNA).

The snRNPs play a crucial role in the formation of spliceosomes, large ribonucleoprotein complexes that remove introns (non-coding sequences) from pre-mRNA and join exons (coding sequences) together to form mature mRNA. Each snRNP contains a specific snRNA molecule, such as U1, U2, U4, U5, or U6, which recognizes and binds to specific sequences within the pre-mRNA during splicing. The associated proteins help stabilize the snRNP structure and facilitate its interactions with other components of the spliceosome.

In addition to their role in splicing, some snRNPs are also involved in other cellular processes, such as transcription regulation, RNA export, and DNA damage response. Dysregulation or mutations in snRNP components have been implicated in various human diseases, including cancer, neurological disorders, and autoimmune diseases.

Beta 2-glycoprotein I, also known as apolipoprotein H, is a plasma protein that belongs to the family of proteins called immunoglobulin-binding proteins. It has a molecular weight of approximately 44 kDa and is composed of five domains with similar structures.

Beta 2-glycoprotein I is primarily produced in the liver and circulates in the bloodstream, where it plays a role in several physiological processes, including coagulation, complement activation, and lipid metabolism. It has been identified as an autoantigen in certain autoimmune disorders, such as antiphospholipid syndrome (APS), where autoantibodies against beta 2-glycoprotein I can cause blood clots, miscarriages, and other complications.

In medical terminology, the definition of "beta 2-glycoprotein I" is as follows:

A plasma protein that belongs to the family of immunoglobulin-binding proteins and has a molecular weight of approximately 44 kDa. It is primarily produced in the liver and circulates in the bloodstream, where it plays a role in several physiological processes, including coagulation, complement activation, and lipid metabolism. Autoantibodies against beta 2-glycoprotein I are associated with certain autoimmune disorders, such as antiphospholipid syndrome (APS), where they can cause blood clots, miscarriages, and other complications.

A biological marker, often referred to as a biomarker, is a measurable indicator that reflects the presence or severity of a disease state, or a response to a therapeutic intervention. Biomarkers can be found in various materials such as blood, tissues, or bodily fluids, and they can take many forms, including molecular, histologic, radiographic, or physiological measurements.

In the context of medical research and clinical practice, biomarkers are used for a variety of purposes, such as:

1. Diagnosis: Biomarkers can help diagnose a disease by indicating the presence or absence of a particular condition. For example, prostate-specific antigen (PSA) is a biomarker used to detect prostate cancer.
2. Monitoring: Biomarkers can be used to monitor the progression or regression of a disease over time. For instance, hemoglobin A1c (HbA1c) levels are monitored in diabetes patients to assess long-term blood glucose control.
3. Predicting: Biomarkers can help predict the likelihood of developing a particular disease or the risk of a negative outcome. For example, the presence of certain genetic mutations can indicate an increased risk for breast cancer.
4. Response to treatment: Biomarkers can be used to evaluate the effectiveness of a specific treatment by measuring changes in the biomarker levels before and after the intervention. This is particularly useful in personalized medicine, where treatments are tailored to individual patients based on their unique biomarker profiles.

It's important to note that for a biomarker to be considered clinically valid and useful, it must undergo rigorous validation through well-designed studies, including demonstrating sensitivity, specificity, reproducibility, and clinical relevance.

The complement system is a group of proteins found in the blood and on the surface of cells that when activated, work together to help eliminate pathogens such as bacteria, viruses, and fungi from the body. The proteins are normally inactive in the bloodstream. When they encounter an invading microorganism or foreign substance, a series of reactions take place leading to the activation of the complement system. Activation results in the production of effector molecules that can punch holes in the cell membranes of pathogens, recruit and activate immune cells, and help remove debris and dead cells from the body.

There are three main pathways that can lead to complement activation: the classical pathway, the lectin pathway, and the alternative pathway. Each pathway involves a series of proteins that work together in a cascade-like manner to amplify the response and generate effector molecules. The three main effector molecules produced by the complement system are C3b, C4b, and C5b. These molecules can bind to the surface of pathogens, marking them for destruction by other immune cells.

Complement proteins also play a role in the regulation of the immune response. They help to prevent excessive activation of the complement system, which could damage host tissues. Dysregulation of the complement system has been implicated in a number of diseases, including autoimmune disorders and inflammatory conditions.

In summary, Complement System Proteins are a group of proteins that play a crucial role in the immune response by helping to eliminate pathogens and regulate the immune response. They can be activated through three different pathways, leading to the production of effector molecules that mark pathogens for destruction. Dysregulation of the complement system has been linked to various diseases.

Vasculitis is a group of disorders characterized by inflammation of the blood vessels, which can cause changes in the vessel walls including thickening, narrowing, or weakening. These changes can restrict blood flow, leading to organ and tissue damage. The specific symptoms and severity of vasculitis depend on the size and location of the affected blood vessels and the extent of inflammation. Vasculitis can affect any organ system in the body, and its causes can vary, including infections, autoimmune disorders, or exposure to certain medications or chemicals.

Antibody specificity refers to the ability of an antibody to bind to a specific epitope or antigenic determinant on an antigen. Each antibody has a unique structure that allows it to recognize and bind to a specific region of an antigen, typically a small portion of the antigen's surface made up of amino acids or sugar residues. This highly specific binding is mediated by the variable regions of the antibody's heavy and light chains, which form a pocket that recognizes and binds to the epitope.

The specificity of an antibody is determined by its unique complementarity-determining regions (CDRs), which are loops of amino acids located in the variable domains of both the heavy and light chains. The CDRs form a binding site that recognizes and interacts with the epitope on the antigen. The precise fit between the antibody's binding site and the epitope is critical for specificity, as even small changes in the structure of either can prevent binding.

Antibody specificity is important in immune responses because it allows the immune system to distinguish between self and non-self antigens. This helps to prevent autoimmune reactions where the immune system attacks the body's own cells and tissues. Antibody specificity also plays a crucial role in diagnostic tests, such as ELISA assays, where antibodies are used to detect the presence of specific antigens in biological samples.

T-lymphocytes, also known as T-cells, are a type of white blood cell that plays a key role in the adaptive immune system's response to infection. They are produced in the bone marrow and mature in the thymus gland. There are several different types of T-cells, including CD4+ helper T-cells, CD8+ cytotoxic T-cells, and regulatory T-cells (Tregs).

CD4+ helper T-cells assist in activating other immune cells, such as B-lymphocytes and macrophages. They also produce cytokines, which are signaling molecules that help coordinate the immune response. CD8+ cytotoxic T-cells directly kill infected cells by releasing toxic substances. Regulatory T-cells help maintain immune tolerance and prevent autoimmune diseases by suppressing the activity of other immune cells.

T-lymphocytes are important in the immune response to viral infections, cancer, and other diseases. Dysfunction or depletion of T-cells can lead to immunodeficiency and increased susceptibility to infections. On the other hand, an overactive T-cell response can contribute to autoimmune diseases and chronic inflammation.

Cryoglobulins are immunoglobulins (a type of antibody) that precipitate or become insoluble at reduced temperatures, typically below 37°C (98.6°F), and re-dissolve when rewarmed. They can be found in various clinical conditions such as infections, inflammatory diseases, and lymphoproliferative disorders.

The presence of cryoglobulins in the blood can lead to a variety of symptoms, including purpura (a type of skin rash), arthralgias (joint pain), neuropathy (nerve damage), and glomerulonephritis (kidney inflammation). The diagnosis of cryoglobulinemia is made by detecting the presence of cryoglobulins in the serum, which requires special handling and processing of the blood sample. Treatment of cryoglobulinemia depends on the underlying cause and may include medications such as corticosteroids, immunosuppressive agents, or targeted therapies.

Proteinuria is a medical term that refers to the presence of excess proteins, particularly albumin, in the urine. Under normal circumstances, only small amounts of proteins should be found in the urine because the majority of proteins are too large to pass through the glomeruli, which are the filtering units of the kidneys.

However, when the glomeruli become damaged or diseased, they may allow larger molecules such as proteins to leak into the urine. Persistent proteinuria is often a sign of kidney disease and can indicate damage to the glomeruli. It is usually detected through a routine urinalysis and may be confirmed with further testing.

The severity of proteinuria can vary, and it can be a symptom of various underlying conditions such as diabetes, hypertension, glomerulonephritis, and other kidney diseases. Treatment for proteinuria depends on the underlying cause and may include medications to control blood pressure, manage diabetes, or reduce protein loss in the urine.

The adrenal cortex hormones are a group of steroid hormones produced and released by the outer portion (cortex) of the adrenal glands, which are located on top of each kidney. These hormones play crucial roles in regulating various physiological processes, including:

1. Glucose metabolism: Cortisol helps control blood sugar levels by increasing glucose production in the liver and reducing its uptake in peripheral tissues.
2. Protein and fat metabolism: Cortisol promotes protein breakdown and fatty acid mobilization, providing essential building blocks for energy production during stressful situations.
3. Immune response regulation: Cortisol suppresses immune function to prevent overactivation and potential damage to the body during stress.
4. Cardiovascular function: Aldosterone regulates electrolyte balance and blood pressure by promoting sodium reabsorption and potassium excretion in the kidneys.
5. Sex hormone production: The adrenal cortex produces small amounts of sex hormones, such as androgens and estrogens, which contribute to sexual development and function.
6. Growth and development: Cortisol plays a role in normal growth and development by influencing the activity of growth-promoting hormones like insulin-like growth factor 1 (IGF-1).

The main adrenal cortex hormones include:

1. Glucocorticoids: Cortisol is the primary glucocorticoid, responsible for regulating metabolism and stress response.
2. Mineralocorticoids: Aldosterone is the primary mineralocorticoid, involved in electrolyte balance and blood pressure regulation.
3. Androgens: Dehydroepiandrosterone (DHEA) and its sulfate derivative (DHEAS) are the most abundant adrenal androgens, contributing to sexual development and function.
4. Estrogens: Small amounts of estrogens are produced by the adrenal cortex, mainly in women.

Disorders related to impaired adrenal cortex hormone production or regulation can lead to various clinical manifestations, such as Addison's disease (adrenal insufficiency), Cushing's syndrome (hypercortisolism), and congenital adrenal hyperplasia (CAH).

IgG receptors, also known as Fcγ receptors (Fc gamma receptors), are specialized protein molecules found on the surface of various immune cells, such as neutrophils, monocytes, macrophages, and some lymphocytes. These receptors recognize and bind to the Fc region of IgG antibodies, one of the five classes of immunoglobulins in the human body.

IgG receptors play a crucial role in immune responses by mediating different effector functions, including:

1. Antibody-dependent cellular cytotoxicity (ADCC): IgG receptors on natural killer (NK) cells and other immune cells bind to IgG antibodies coated on the surface of virus-infected or cancer cells, leading to their destruction.
2. Phagocytosis: When IgG antibodies tag pathogens or foreign particles, phagocytes like neutrophils and macrophages recognize and bind to these immune complexes via IgG receptors, facilitating the engulfment and removal of the targeted particles.
3. Antigen presentation: IgG receptors on antigen-presenting cells (APCs) can internalize immune complexes, process the antigens, and present them to T cells, thereby initiating adaptive immune responses.
4. Inflammatory response regulation: IgG receptors can modulate inflammation by activating or inhibiting downstream signaling pathways in immune cells, depending on the specific type of Fcγ receptor and its activation state.

There are several types of IgG receptors (FcγRI, FcγRII, FcγRIII, and FcγRIV) with varying affinities for different subclasses of IgG antibodies (IgG1, IgG2, IgG3, and IgG4). The distinct functions and expression patterns of these receptors contribute to the complexity and fine-tuning of immune responses in the human body.

Plasmapheresis is a medical procedure where the liquid portion of the blood (plasma) is separated from the blood cells. The plasma, which may contain harmful substances such as antibodies or toxins, is then removed and replaced with fresh plasma or a plasma substitute. The remaining blood cells are mixed with the new plasma and returned to the body. This process is also known as therapeutic plasma exchange (TPE). It's used to treat various medical conditions including certain autoimmune diseases, poisonings, and neurological disorders.

Azathioprine is an immunosuppressive medication that is used to prevent the rejection of transplanted organs and to treat autoimmune diseases such as rheumatoid arthritis, lupus, and inflammatory bowel disease. It works by suppressing the activity of the immune system, which helps to reduce inflammation and prevent the body from attacking its own tissues.

Azathioprine is a prodrug that is converted into its active form, 6-mercaptopurine, in the body. This medication can have significant side effects, including decreased white blood cell count, increased risk of infection, and liver damage. It may also increase the risk of certain types of cancer, particularly skin cancer and lymphoma.

Healthcare professionals must carefully monitor patients taking azathioprine for these potential side effects. They may need to adjust the dosage or stop the medication altogether if serious side effects occur. Patients should also take steps to reduce their risk of infection and skin cancer, such as practicing good hygiene, avoiding sun exposure, and using sunscreen.

Methylprednisolone is a synthetic glucocorticoid drug, which is a class of hormones that naturally occur in the body and are produced by the adrenal gland. It is often used to treat various medical conditions such as inflammation, allergies, and autoimmune disorders. Methylprednisolone works by reducing the activity of the immune system, which helps to reduce symptoms such as swelling, pain, and redness.

Methylprednisolone is available in several forms, including tablets, oral suspension, and injectable solutions. It may be used for short-term or long-term treatment, depending on the condition being treated. Common side effects of methylprednisolone include increased appetite, weight gain, insomnia, mood changes, and increased susceptibility to infections. Long-term use of methylprednisolone can lead to more serious side effects such as osteoporosis, cataracts, and adrenal suppression.

It is important to note that methylprednisolone should be used under the close supervision of a healthcare provider, as it can cause serious side effects if not used properly. The dosage and duration of treatment will depend on various factors such as the patient's age, weight, medical history, and the condition being treated.

Interferon Regulatory Factors (IRFs) are a family of transcription factors that play crucial roles in the regulation of immune responses, particularly in the expression of interferons (IFNs) and other genes involved in innate immunity and inflammation. In humans, there are nine known IRF proteins (IRF1-9), each with distinct functions and patterns of expression.

The primary function of IRFs is to regulate the transcription of type I IFNs (IFN-α and IFN-β) and other immune response genes in response to various stimuli, such as viral infections, bacterial components, and proinflammatory cytokines. IRFs can either activate or repress gene expression by binding to specific DNA sequences called interferon-stimulated response elements (ISREs) and/or IFN consensus sequences (ICSs) in the promoter regions of target genes.

IRF1, IRF3, and IRF7 are primarily involved in type I IFN regulation, with IRF1 acting as a transcriptional activator for IFN-β and various ISRE-containing genes, while IRF3 and IRF7 function as master regulators of the type I IFN response to viral infections. Upon viral recognition by pattern recognition receptors (PRRs), IRF3 and IRF7 are activated through phosphorylation and translocate to the nucleus, where they induce the expression of type I IFNs and other antiviral genes.

IRF2, IRF4, IRF5, and IRF8 have more diverse roles in immune regulation, including the control of T-cell differentiation, B-cell development, and myeloid cell function. For example, IRF4 is essential for the development and function of Th2 cells, while IRF5 and IRF8 are involved in the differentiation of dendritic cells and macrophages.

IRF6 and IRF9 have unique functions compared to other IRFs. IRF6 is primarily involved in epithelial cell development and differentiation, while IRF9 forms a complex with STAT1 and STAT2 to regulate the transcription of IFN-stimulated genes (ISGs) during the type I IFN response.

In summary, IRFs are a family of transcription factors that play crucial roles in various aspects of immune regulation, including antiviral responses, T-cell and B-cell development, and myeloid cell function. Dysregulation of IRF activity can lead to the development of autoimmune diseases, chronic inflammation, and cancer.

B-lymphocytes, also known as B-cells, are a type of white blood cell that plays a central role in the humoral immune response. They are responsible for producing antibodies, which are proteins that help to neutralize or destroy pathogens such as viruses and bacteria.

B-lymphocyte subsets refer to distinct populations of B-cells that can be identified based on their surface receptors and functional characteristics. Some common B-lymphocyte subsets include:

1. Naive B-cells: These are mature B-cells that have not yet been exposed to an antigen. They express surface receptors called immunoglobulin M (IgM) and immunoglobulin D (IgD).
2. Memory B-cells: These are B-cells that have previously encountered an antigen and mounted an immune response. They express high levels of surface immunoglobulins and can quickly differentiate into antibody-secreting plasma cells upon re-exposure to the same antigen.
3. Plasma cells: These are fully differentiated B-cells that secrete large amounts of antibodies in response to an antigen. They lack surface immunoglobulins and do not undergo further division.
4. Regulatory B-cells: These are a subset of B-cells that modulate the immune response by producing anti-inflammatory cytokines and suppressing the activation of other immune cells.
5. B-1 cells: These are a population of B-cells that are primarily found in the peripheral blood and mucosal tissues. They produce natural antibodies that provide early protection against pathogens and help to maintain tissue homeostasis.

Understanding the different B-lymphocyte subsets and their functions is important for diagnosing and treating immune-related disorders, including autoimmune diseases, infections, and cancer.

Single Nucleotide Polymorphism (SNP) is a type of genetic variation that occurs when a single nucleotide (A, T, C, or G) in the DNA sequence is altered. This alteration must occur in at least 1% of the population to be considered a SNP. These variations can help explain why some people are more susceptible to certain diseases than others and can also influence how an individual responds to certain medications. SNPs can serve as biological markers, helping scientists locate genes that are associated with disease. They can also provide information about an individual's ancestry and ethnic background.

Complement C4b is a protein fragment that is formed during the activation of the complement system, which is a part of the immune system. The complement system helps to eliminate pathogens and damaged cells from the body by tagging them for destruction and attracting immune cells to the site of infection or injury.

C4b is generated when the C4 protein is cleaved into two smaller fragments, C4a and C4b, during the activation of the classical or lectin pathways of the complement system. C4b then binds covalently to the surface of the target cell or pathogen, forming a complex with other complement proteins that can create a membrane attack complex (MAC) and cause cell lysis.

C4b can also act as an opsonin, coating the surface of the target cell or pathogen and making it easier for immune cells to recognize and phagocytose them. Additionally, C4b can activate the alternative pathway of the complement system, leading to further amplification of the complement response.

Prednisone is a synthetic glucocorticoid, which is a type of corticosteroid hormone. It is primarily used to reduce inflammation in various conditions such as asthma, allergies, arthritis, and autoimmune disorders. Prednisone works by mimicking the effects of natural hormones produced by the adrenal glands, suppressing the immune system's response and reducing the release of substances that cause inflammation.

It is available in oral tablet form and is typically prescribed to be taken at specific times during the day, depending on the condition being treated. Common side effects of prednisone include increased appetite, weight gain, mood changes, insomnia, and easy bruising. Long-term use or high doses can lead to more serious side effects such as osteoporosis, diabetes, cataracts, and increased susceptibility to infections.

Healthcare providers closely monitor patients taking prednisone for extended periods to minimize the risk of adverse effects. It is essential to follow the prescribed dosage regimen and not discontinue the medication abruptly without medical supervision, as this can lead to withdrawal symptoms or a rebound of the underlying condition.

Antibodies are proteins produced by the immune system in response to the presence of a foreign substance, such as a bacterium or virus. They are capable of identifying and binding to specific antigens (foreign substances) on the surface of these invaders, marking them for destruction by other immune cells. Antibodies are also known as immunoglobulins and come in several different types, including IgA, IgD, IgE, IgG, and IgM, each with a unique function in the immune response. They are composed of four polypeptide chains, two heavy chains and two light chains, that are held together by disulfide bonds. The variable regions of the heavy and light chains form the antigen-binding site, which is specific to a particular antigen.

Complement C2 is a protein that plays a crucial role in the complement system, which is a part of the immune system that helps to eliminate pathogens and damaged cells from the body. Specifically, C2 is a component of the classical complement pathway, which is activated by the binding of antibodies to antigens on the surface of foreign particles or cells.

When the classical pathway is activated, C2 is cleaved into two fragments: C2a and C2b. C2a then binds to C4b to form the C3 convertase (C4b2a), which cleaves C3 into C3a and C3b. C3b can then go on to form the membrane attack complex, which creates a pore in the membrane of the target cell, leading to its lysis.

In summary, Complement C2 is a protein that helps to activate the complement system and destroy foreign particles or cells through the formation of the C3 convertase and the membrane attack complex.

Lymphocyte activation is the process by which B-cells and T-cells (types of lymphocytes) become activated to perform effector functions in an immune response. This process involves the recognition of specific antigens presented on the surface of antigen-presenting cells, such as dendritic cells or macrophages.

The activation of B-cells leads to their differentiation into plasma cells that produce antibodies, while the activation of T-cells results in the production of cytotoxic T-cells (CD8+ T-cells) that can directly kill infected cells or helper T-cells (CD4+ T-cells) that assist other immune cells.

Lymphocyte activation involves a series of intracellular signaling events, including the binding of co-stimulatory molecules and the release of cytokines, which ultimately result in the expression of genes involved in cell proliferation, differentiation, and effector functions. The activation process is tightly regulated to prevent excessive or inappropriate immune responses that can lead to autoimmunity or chronic inflammation.

Glucocorticoids are a class of steroid hormones that are naturally produced in the adrenal gland, or can be synthetically manufactured. They play an essential role in the metabolism of carbohydrates, proteins, and fats, and have significant anti-inflammatory effects. Glucocorticoids suppress immune responses and inflammation by inhibiting the release of inflammatory mediators from various cells, such as mast cells, eosinophils, and lymphocytes. They are frequently used in medical treatment for a wide range of conditions, including allergies, asthma, rheumatoid arthritis, dermatological disorders, and certain cancers. Prolonged use or high doses of glucocorticoids can lead to several side effects, such as weight gain, mood changes, osteoporosis, and increased susceptibility to infections.

Monoclonal antibodies are a type of antibody that are identical because they are produced by a single clone of cells. They are laboratory-produced molecules that act like human antibodies in the immune system. They can be designed to attach to specific proteins found on the surface of cancer cells, making them useful for targeting and treating cancer. Monoclonal antibodies can also be used as a therapy for other diseases, such as autoimmune disorders and inflammatory conditions.

Monoclonal antibodies are produced by fusing a single type of immune cell, called a B cell, with a tumor cell to create a hybrid cell, or hybridoma. This hybrid cell is then able to replicate indefinitely, producing a large number of identical copies of the original antibody. These antibodies can be further modified and engineered to enhance their ability to bind to specific targets, increase their stability, and improve their effectiveness as therapeutic agents.

Monoclonal antibodies have several mechanisms of action in cancer therapy. They can directly kill cancer cells by binding to them and triggering an immune response. They can also block the signals that promote cancer growth and survival. Additionally, monoclonal antibodies can be used to deliver drugs or radiation directly to cancer cells, increasing the effectiveness of these treatments while minimizing their side effects on healthy tissues.

Monoclonal antibodies have become an important tool in modern medicine, with several approved for use in cancer therapy and other diseases. They are continuing to be studied and developed as a promising approach to treating a wide range of medical conditions.

Transverse Myelitis is a neurological disorder that involves inflammation of the spinal cord, leading to damage in both sides of the cord. This results in varying degrees of motor, sensory, and autonomic dysfunction, typically defined by the level of the spine that's affected. Symptoms may include a sudden onset of lower back pain, muscle weakness, paraesthesia or loss of sensation, and bowel/bladder dysfunction. The exact cause is often unknown but can be associated with infections, autoimmune disorders, or other underlying conditions.

A kidney, in medical terms, is one of two bean-shaped organs located in the lower back region of the body. They are essential for maintaining homeostasis within the body by performing several crucial functions such as:

1. Regulation of water and electrolyte balance: Kidneys help regulate the amount of water and various electrolytes like sodium, potassium, and calcium in the bloodstream to maintain a stable internal environment.

2. Excretion of waste products: They filter waste products from the blood, including urea (a byproduct of protein metabolism), creatinine (a breakdown product of muscle tissue), and other harmful substances that result from normal cellular functions or external sources like medications and toxins.

3. Endocrine function: Kidneys produce several hormones with important roles in the body, such as erythropoietin (stimulates red blood cell production), renin (regulates blood pressure), and calcitriol (activated form of vitamin D that helps regulate calcium homeostasis).

4. pH balance regulation: Kidneys maintain the proper acid-base balance in the body by excreting either hydrogen ions or bicarbonate ions, depending on whether the blood is too acidic or too alkaline.

5. Blood pressure control: The kidneys play a significant role in regulating blood pressure through the renin-angiotensin-aldosterone system (RAAS), which constricts blood vessels and promotes sodium and water retention to increase blood volume and, consequently, blood pressure.

Anatomically, each kidney is approximately 10-12 cm long, 5-7 cm wide, and 3 cm thick, with a weight of about 120-170 grams. They are surrounded by a protective layer of fat and connected to the urinary system through the renal pelvis, ureters, bladder, and urethra.

Anti-idiotypic antibodies are a type of immune protein that recognizes and binds to the unique identifying region (idiotype) of another antibody. These antibodies are produced by the immune system as part of a regulatory feedback mechanism, where they can modulate or inhibit the activity of the original antibody. They have been studied for their potential use in immunotherapy and vaccine development.

Skin diseases, also known as dermatological conditions, refer to any medical condition that affects the skin, which is the largest organ of the human body. These diseases can affect the skin's function, appearance, or overall health. They can be caused by various factors, including genetics, infections, allergies, environmental factors, and aging.

Skin diseases can present in many different forms, such as rashes, blisters, sores, discolorations, growths, or changes in texture. Some common examples of skin diseases include acne, eczema, psoriasis, dermatitis, fungal infections, viral infections, bacterial infections, and skin cancer.

The symptoms and severity of skin diseases can vary widely depending on the specific condition and individual factors. Some skin diseases are mild and can be treated with over-the-counter medications or topical creams, while others may require more intensive treatments such as prescription medications, light therapy, or even surgery.

It is important to seek medical attention if you experience any unusual or persistent changes in your skin, as some skin diseases can be serious or indicative of other underlying health conditions. A dermatologist is a medical doctor who specializes in the diagnosis and treatment of skin diseases.

Medical Definition:

"Risk factors" are any attribute, characteristic or exposure of an individual that increases the likelihood of developing a disease or injury. They can be divided into modifiable and non-modifiable risk factors. Modifiable risk factors are those that can be changed through lifestyle choices or medical treatment, while non-modifiable risk factors are inherent traits such as age, gender, or genetic predisposition. Examples of modifiable risk factors include smoking, alcohol consumption, physical inactivity, and unhealthy diet, while non-modifiable risk factors include age, sex, and family history. It is important to note that having a risk factor does not guarantee that a person will develop the disease, but rather indicates an increased susceptibility.

Genotype, in genetics, refers to the complete heritable genetic makeup of an individual organism, including all of its genes. It is the set of instructions contained in an organism's DNA for the development and function of that organism. The genotype is the basis for an individual's inherited traits, and it can be contrasted with an individual's phenotype, which refers to the observable physical or biochemical characteristics of an organism that result from the expression of its genes in combination with environmental influences.

It is important to note that an individual's genotype is not necessarily identical to their genetic sequence. Some genes have multiple forms called alleles, and an individual may inherit different alleles for a given gene from each parent. The combination of alleles that an individual inherits for a particular gene is known as their genotype for that gene.

Understanding an individual's genotype can provide important information about their susceptibility to certain diseases, their response to drugs and other treatments, and their risk of passing on inherited genetic disorders to their offspring.

A kidney glomerulus is a functional unit in the nephron of the kidney. It is a tuft of capillaries enclosed within a structure called Bowman's capsule, which filters waste and excess fluids from the blood. The glomerulus receives blood from an afferent arteriole and drains into an efferent arteriole.

The process of filtration in the glomerulus is called ultrafiltration, where the pressure within the glomerular capillaries drives plasma fluid and small molecules (such as ions, glucose, amino acids, and waste products) through the filtration membrane into the Bowman's space. Larger molecules, like proteins and blood cells, are retained in the blood due to their larger size. The filtrate then continues down the nephron for further processing, eventually forming urine.

Hemolytic anemia, autoimmune is a type of anemia characterized by the premature destruction of red blood cells (RBCs) in which the immune system mistakenly attacks and destroys its own RBCs. This occurs when the body produces autoantibodies that bind to the surface of RBCs, leading to their rupture (hemolysis). The symptoms may include fatigue, weakness, shortness of breath, and dark colored urine. The diagnosis is made through blood tests that measure the number and size of RBCs, reticulocyte count, and the presence of autoantibodies. Treatment typically involves suppressing the immune system with medications such as corticosteroids or immunosuppressive drugs, and sometimes removal of the spleen (splenectomy) may be necessary.

Interferon-alpha (IFN-α) is a type I interferon, which is a group of signaling proteins made and released by host cells in response to the presence of viruses, parasites, and tumor cells. It plays a crucial role in the immune response against viral infections. IFN-α has antiviral, immunomodulatory, and anti-proliferative effects.

IFN-α is produced naturally by various cell types, including leukocytes (white blood cells), fibroblasts, and epithelial cells, in response to viral or bacterial stimulation. It binds to specific receptors on the surface of nearby cells, triggering a signaling cascade that leads to the activation of genes involved in the antiviral response. This results in the production of proteins that inhibit viral replication and promote the presentation of viral antigens to the immune system, enhancing its ability to recognize and eliminate infected cells.

In addition to its role in the immune response, IFN-α has been used as a therapeutic agent for various medical conditions, including certain types of cancer, chronic hepatitis B and C, and multiple sclerosis. However, its use is often limited by side effects such as flu-like symptoms, depression, and neuropsychiatric disorders.

Animal disease models are specialized animals, typically rodents such as mice or rats, that have been genetically engineered or exposed to certain conditions to develop symptoms and physiological changes similar to those seen in human diseases. These models are used in medical research to study the pathophysiology of diseases, identify potential therapeutic targets, test drug efficacy and safety, and understand disease mechanisms.

The genetic modifications can include knockout or knock-in mutations, transgenic expression of specific genes, or RNA interference techniques. The animals may also be exposed to environmental factors such as chemicals, radiation, or infectious agents to induce the disease state.

Examples of animal disease models include:

1. Mouse models of cancer: Genetically engineered mice that develop various types of tumors, allowing researchers to study cancer initiation, progression, and metastasis.
2. Alzheimer's disease models: Transgenic mice expressing mutant human genes associated with Alzheimer's disease, which exhibit amyloid plaque formation and cognitive decline.
3. Diabetes models: Obese and diabetic mouse strains like the NOD (non-obese diabetic) or db/db mice, used to study the development of type 1 and type 2 diabetes, respectively.
4. Cardiovascular disease models: Atherosclerosis-prone mice, such as ApoE-deficient or LDLR-deficient mice, that develop plaque buildup in their arteries when fed a high-fat diet.
5. Inflammatory bowel disease models: Mice with genetic mutations affecting intestinal barrier function and immune response, such as IL-10 knockout or SAMP1/YitFc mice, which develop colitis.

Animal disease models are essential tools in preclinical research, but it is important to recognize their limitations. Differences between species can affect the translatability of results from animal studies to human patients. Therefore, researchers must carefully consider the choice of model and interpret findings cautiously when applying them to human diseases.

A cohort study is a type of observational study in which a group of individuals who share a common characteristic or exposure are followed up over time to determine the incidence of a specific outcome or outcomes. The cohort, or group, is defined based on the exposure status (e.g., exposed vs. unexposed) and then monitored prospectively to assess for the development of new health events or conditions.

Cohort studies can be either prospective or retrospective in design. In a prospective cohort study, participants are enrolled and followed forward in time from the beginning of the study. In contrast, in a retrospective cohort study, researchers identify a cohort that has already been assembled through medical records, insurance claims, or other sources and then look back in time to assess exposure status and health outcomes.

Cohort studies are useful for establishing causality between an exposure and an outcome because they allow researchers to observe the temporal relationship between the two. They can also provide information on the incidence of a disease or condition in different populations, which can be used to inform public health policy and interventions. However, cohort studies can be expensive and time-consuming to conduct, and they may be subject to bias if participants are not representative of the population or if there is loss to follow-up.

Flow cytometry is a medical and research technique used to measure physical and chemical characteristics of cells or particles, one cell at a time, as they flow in a fluid stream through a beam of light. The properties measured include:

* Cell size (light scatter)
* Cell internal complexity (granularity, also light scatter)
* Presence or absence of specific proteins or other molecules on the cell surface or inside the cell (using fluorescent antibodies or other fluorescent probes)

The technique is widely used in cell counting, cell sorting, protein engineering, biomarker discovery and monitoring disease progression, particularly in hematology, immunology, and cancer research.

Tumor Necrosis Factor Ligand Superfamily Member 13 (TNFSF13), also known as APRIL (A Proliferation-Inducing Ligand), is a type II transmembrane protein and a member of the tumor necrosis factor (TNF) ligand superfamily. It plays a crucial role in the immune system, particularly in the activation, proliferation, and differentiation of B cells, which are key players in the humoral immune response.

TNFSF13 is expressed by various cell types, including macrophages, dendritic cells, and neutrophils. It binds to two receptors: TACI (Transmembrane Activator and Calcium Modulator and Cyclophilin Ligand Interactor) and BCMA (B-cell Maturation Antigen), which are primarily found on the surface of B cells. The interaction between TNFSF13 and its receptors promotes the survival, proliferation, and differentiation of B cells into plasma cells, ultimately leading to increased antibody production.

Dysregulation of TNFSF13 has been implicated in several autoimmune and inflammatory diseases, such as rheumatoid arthritis, systemic lupus erythematosus (SLE), and multiple sclerosis (MS). Therefore, targeting this molecule or its signaling pathways has been a focus of research for the development of novel therapeutic strategies in these conditions.

Thrombocytopenia is a medical condition characterized by an abnormally low platelet count (thrombocytes) in the blood. Platelets are small cell fragments that play a crucial role in blood clotting, helping to stop bleeding when a blood vessel is damaged. A healthy adult typically has a platelet count between 150,000 and 450,000 platelets per microliter of blood. Thrombocytopenia is usually diagnosed when the platelet count falls below 150,000 platelets/µL.

Thrombocytopenia can be classified into three main categories based on its underlying cause:

1. Immune thrombocytopenia (ITP): An autoimmune disorder where the immune system mistakenly attacks and destroys its own platelets, leading to a decreased platelet count. ITP can be further divided into primary or secondary forms, depending on whether it occurs alone or as a result of another medical condition or medication.
2. Decreased production: Thrombocytopenia can occur when there is insufficient production of platelets in the bone marrow due to various causes, such as viral infections, chemotherapy, radiation therapy, leukemia, aplastic anemia, or vitamin B12 or folate deficiency.
3. Increased destruction or consumption: Thrombocytopenia can also result from increased platelet destruction or consumption due to conditions like disseminated intravascular coagulation (DIC), thrombotic thrombocytopenic purpura (TTP), hemolytic uremic syndrome (HUS), or severe bacterial infections.

Symptoms of thrombocytopenia may include easy bruising, prolonged bleeding from cuts, spontaneous nosebleeds, bleeding gums, blood in urine or stools, and skin rashes like petechiae (small red or purple spots) or purpura (larger patches). The severity of symptoms can vary depending on the degree of thrombocytopenia and the presence of any underlying conditions. Treatment for thrombocytopenia depends on the cause and may include medications, transfusions, or addressing the underlying condition.

An allele is a variant form of a gene that is located at a specific position on a specific chromosome. Alleles are alternative forms of the same gene that arise by mutation and are found at the same locus or position on homologous chromosomes.

Each person typically inherits two copies of each gene, one from each parent. If the two alleles are identical, a person is said to be homozygous for that trait. If the alleles are different, the person is heterozygous.

For example, the ABO blood group system has three alleles, A, B, and O, which determine a person's blood type. If a person inherits two A alleles, they will have type A blood; if they inherit one A and one B allele, they will have type AB blood; if they inherit two B alleles, they will have type B blood; and if they inherit two O alleles, they will have type O blood.

Alleles can also influence traits such as eye color, hair color, height, and other physical characteristics. Some alleles are dominant, meaning that only one copy of the allele is needed to express the trait, while others are recessive, meaning that two copies of the allele are needed to express the trait.

Genetic polymorphism refers to the occurrence of multiple forms (called alleles) of a particular gene within a population. These variations in the DNA sequence do not generally affect the function or survival of the organism, but they can contribute to differences in traits among individuals. Genetic polymorphisms can be caused by single nucleotide changes (SNPs), insertions or deletions of DNA segments, or other types of genetic rearrangements. They are important for understanding genetic diversity and evolution, as well as for identifying genetic factors that may contribute to disease susceptibility in humans.

Complement receptor 3b (CR3b or CD11b/CD18) is not a medical definition itself, but I can provide you with the relevant information regarding this term.

Complement receptor 3 (CR3) is a heterodimeric receptor consisting of two subunits, CD11b (also known as Mac-1 or CR3 alpha) and CD18 (also known as beta2 integrin). There are two forms of the CD11b/CD18 heterodimer: CR3a (CD11b/CD18) and CR3b (CD11b/CD18'). The difference between these two forms lies in the conformation of the CD11b subunit.

Complement receptor 3b (CR3b or CD11b/CD18') is a less common form of the CR3 receptor, which is primarily expressed on myeloid cells such as monocytes, macrophages, and neutrophils. CR3b has a higher affinity for complement component C3b and its fragments iC3b and C3dg compared to CR3a.

CR3b plays a role in various immune functions, including:

1. Phagocytosis: Binding of C3b or its fragments to CR3b facilitates the recognition and uptake of opsonized pathogens by phagocytes.
2. Adhesion: The integrin component of CR3b mediates cell-cell and cell-matrix interactions, contributing to leukocyte migration and recruitment to sites of inflammation or infection.
3. Intracellular signaling: Activation of CR3b can lead to intracellular signaling events that modulate immune responses, such as the release of pro-inflammatory cytokines and reactive oxygen species.

In summary, Complement receptor 3b (CR3b or CD11b/CD18') is a less common form of CR3 primarily expressed on myeloid cells that binds complement component C3b and its fragments with high affinity, mediating phagocytosis, adhesion, and intracellular signaling.

The term "European Continental Ancestry Group" is a medical/ethnic classification that refers to individuals who trace their genetic ancestry to the continent of Europe. This group includes people from various ethnic backgrounds and nationalities, such as Northern, Southern, Eastern, and Western European descent. It is often used in research and medical settings for population studies or to identify genetic patterns and predispositions to certain diseases that may be more common in specific ancestral groups. However, it's important to note that this classification can oversimplify the complex genetic diversity within and between populations, and should be used with caution.

Blood sedimentation, also known as erythrocyte sedimentation rate (ESR), is a medical test that measures the rate at which red blood cells settle at the bottom of a tube of unclotted blood over a specific period of time. The test is used to detect and monitor inflammation in the body.

During an acute inflammatory response, certain proteins in the blood, such as fibrinogen, increase in concentration. These proteins cause red blood cells to stick together and form rouleaux (stacks of disc-shaped cells). As a result, the red blood cells settle more quickly, leading to a higher ESR.

The ESR test is a non-specific test, meaning that it does not identify the specific cause of inflammation. However, it can be used as an indicator of underlying conditions such as infections, autoimmune diseases, and cancer. The test is also used to monitor the effectiveness of treatment for these conditions.

The ESR test is usually performed by drawing a sample of blood into a special tube and allowing it to sit undisturbed for one hour. The distance that the red blood cells have settled is then measured and recorded as the ESR. Normal values for ESR vary depending on age and gender, with higher values indicating greater inflammation.

Lymphocytes are a type of white blood cell that is an essential part of the immune system. They are responsible for recognizing and responding to potentially harmful substances such as viruses, bacteria, and other foreign invaders. There are two main types of lymphocytes: B-lymphocytes (B-cells) and T-lymphocytes (T-cells).

B-lymphocytes produce antibodies, which are proteins that help to neutralize or destroy foreign substances. When a B-cell encounters a foreign substance, it becomes activated and begins to divide and differentiate into plasma cells, which produce and secrete large amounts of antibodies. These antibodies bind to the foreign substance, marking it for destruction by other immune cells.

T-lymphocytes, on the other hand, are involved in cell-mediated immunity. They directly attack and destroy infected cells or cancerous cells. T-cells can also help to regulate the immune response by producing chemical signals that activate or inhibit other immune cells.

Lymphocytes are produced in the bone marrow and mature in either the bone marrow (B-cells) or the thymus gland (T-cells). They circulate throughout the body in the blood and lymphatic system, where they can be found in high concentrations in lymph nodes, the spleen, and other lymphoid organs.

Abnormalities in the number or function of lymphocytes can lead to a variety of immune-related disorders, including immunodeficiency diseases, autoimmune disorders, and cancer.

Mononuclear leukocytes are a type of white blood cells (leukocytes) that have a single, large nucleus. They include lymphocytes (B-cells, T-cells, and natural killer cells), monocytes, and dendritic cells. These cells play important roles in the body's immune system, including defending against infection and disease, and participating in immune responses and surveillance. Mononuclear leukocytes can be found in the bloodstream as well as in tissues throughout the body. They are involved in both innate and adaptive immunity, providing specific and nonspecific defense mechanisms to protect the body from harmful pathogens and other threats.

A biopsy is a medical procedure in which a small sample of tissue is taken from the body to be examined under a microscope for the presence of disease. This can help doctors diagnose and monitor various medical conditions, such as cancer, infections, or autoimmune disorders. The type of biopsy performed will depend on the location and nature of the suspected condition. Some common types of biopsies include:

1. Incisional biopsy: In this procedure, a surgeon removes a piece of tissue from an abnormal area using a scalpel or other surgical instrument. This type of biopsy is often used when the lesion is too large to be removed entirely during the initial biopsy.

2. Excisional biopsy: An excisional biopsy involves removing the entire abnormal area, along with a margin of healthy tissue surrounding it. This technique is typically employed for smaller lesions or when cancer is suspected.

3. Needle biopsy: A needle biopsy uses a thin, hollow needle to extract cells or fluid from the body. There are two main types of needle biopsies: fine-needle aspiration (FNA) and core needle biopsy. FNA extracts loose cells, while a core needle biopsy removes a small piece of tissue.

4. Punch biopsy: In a punch biopsy, a round, sharp tool is used to remove a small cylindrical sample of skin tissue. This type of biopsy is often used for evaluating rashes or other skin abnormalities.

5. Shave biopsy: During a shave biopsy, a thin slice of tissue is removed from the surface of the skin using a sharp razor-like instrument. This technique is typically used for superficial lesions or growths on the skin.

After the biopsy sample has been collected, it is sent to a laboratory where a pathologist will examine the tissue under a microscope and provide a diagnosis based on their findings. The results of the biopsy can help guide further treatment decisions and determine the best course of action for managing the patient's condition.

Gene frequency, also known as allele frequency, is a measure in population genetics that reflects the proportion of a particular gene or allele (variant of a gene) in a given population. It is calculated as the number of copies of a specific allele divided by the total number of all alleles at that genetic locus in the population.

For example, if we consider a gene with two possible alleles, A and a, the gene frequency of allele A (denoted as p) can be calculated as follows:

p = (number of copies of allele A) / (total number of all alleles at that locus)

Similarly, the gene frequency of allele a (denoted as q) would be:

q = (number of copies of allele a) / (total number of all alleles at that locus)

Since there are only two possible alleles for this gene in this example, p + q = 1. These frequencies can help researchers understand genetic diversity and evolutionary processes within populations.

Immunoglobulin idiotypes refer to the unique antigenic determinants found on the variable regions of an immunoglobulin (antibody) molecule. These determinants are specific to each individual antibody and can be used to distinguish between different antibodies produced by a single individual or between antibodies produced by different individuals.

The variable region of an antibody is responsible for recognizing and binding to a specific antigen. The amino acid sequence in this region varies between different antibodies, and it is these variations that give rise to the unique idiotypes. Idiotypes can be used as markers to study the immune response, including the clonal selection and affinity maturation of B cells during an immune response.

Immunoglobulin idiotypes are also important in the development of monoclonal antibodies for therapeutic use. By identifying and isolating a specific antibody with the desired idiotype, it is possible to produce large quantities of identical antibodies that can be used to treat various diseases, including cancer and autoimmune disorders.

The Fluorescent Antibody Technique (FAT) is a type of immunofluorescence assay used in laboratory medicine and pathology for the detection and localization of specific antigens or antibodies in tissues, cells, or microorganisms. In this technique, a fluorescein-labeled antibody is used to selectively bind to the target antigen or antibody, forming an immune complex. When excited by light of a specific wavelength, the fluorescein label emits light at a longer wavelength, typically visualized as green fluorescence under a fluorescence microscope.

The FAT is widely used in diagnostic microbiology for the identification and characterization of various bacteria, viruses, fungi, and parasites. It has also been applied in the diagnosis of autoimmune diseases and certain cancers by detecting specific antibodies or antigens in patient samples. The main advantage of FAT is its high sensitivity and specificity, allowing for accurate detection and differentiation of various pathogens and disease markers. However, it requires specialized equipment and trained personnel to perform and interpret the results.

Complement C3c is a protein component of the complement system, which is a part of the immune system that helps to clear pathogens and damaged cells from the body. Complement C3c is formed when the third component of the complement system (C3) is cleaved into two smaller proteins, C3a and C3b, during the complement activation process.

C3b can then be further cleaved into C3c and C3dg. C3c is a stable fragment that remains in the circulation and can be measured in blood tests as a marker of complement activation. It plays a role in the opsonization of pathogens, which means it coats them to make them more recognizable to immune cells, and helps to initiate the membrane attack complex (MAC), which forms a pore in the cell membrane of pathogens leading to their lysis or destruction.

Abnormal levels of C3c may indicate an underlying inflammatory or immune-mediated condition, such as infection, autoimmune disease, or cancer.

Rheumatoid factor (RF) is an autoantibody, specifically an immunoglobulin M (IgM) antibody, that can be detected in the blood serum of some people with rheumatoid arthritis (RA), other inflammatory conditions, and infectious diseases. RF targets the Fc portion of IgG, leading to immune complex formation and subsequent inflammation, which contributes to the pathogenesis of RA. However, not all patients with RA test positive for RF, and its presence does not necessarily confirm a diagnosis of RA. Other conditions can also lead to elevated RF levels, such as infections, liver diseases, and certain malignancies. Therefore, the interpretation of RF results should be considered alongside other clinical, laboratory, and imaging findings for an accurate diagnosis and appropriate management.

Immunoglobulins (Igs), also known as antibodies, are glycoprotein molecules produced by the immune system's B cells in response to the presence of foreign substances, such as bacteria, viruses, and toxins. These Y-shaped proteins play a crucial role in identifying and neutralizing pathogens and other antigens, thereby protecting the body against infection and disease.

Immunoglobulins are composed of four polypeptide chains: two identical heavy chains and two identical light chains, held together by disulfide bonds. The variable regions of these chains form the antigen-binding sites, which recognize and bind to specific epitopes on antigens. Based on their heavy chain type, immunoglobulins are classified into five main isotypes or classes: IgA, IgD, IgE, IgG, and IgM. Each class has distinct functions in the immune response, such as providing protection in different body fluids and tissues, mediating hypersensitivity reactions, and aiding in the development of immunological memory.

In medical settings, immunoglobulins can be administered therapeutically to provide passive immunity against certain diseases or to treat immune deficiencies, autoimmune disorders, and other conditions that may benefit from immunomodulation.

A haplotype is a group of genes or DNA sequences that are inherited together from a single parent. It refers to a combination of alleles (variant forms of a gene) that are located on the same chromosome and are usually transmitted as a unit. Haplotypes can be useful in tracing genetic ancestry, understanding the genetic basis of diseases, and developing personalized medical treatments.

In population genetics, haplotypes are often used to study patterns of genetic variation within and between populations. By comparing haplotype frequencies across populations, researchers can infer historical events such as migrations, population expansions, and bottlenecks. Additionally, haplotypes can provide information about the evolutionary history of genes and genomic regions.

In clinical genetics, haplotypes can be used to identify genetic risk factors for diseases or to predict an individual's response to certain medications. For example, specific haplotypes in the HLA gene region have been associated with increased susceptibility to certain autoimmune diseases, while other haplotypes in the CYP450 gene family can affect how individuals metabolize drugs.

Overall, haplotypes provide a powerful tool for understanding the genetic basis of complex traits and diseases, as well as for developing personalized medical treatments based on an individual's genetic makeup.

Thrombosis is the formation of a blood clot (thrombus) inside a blood vessel, obstructing the flow of blood through the circulatory system. When a clot forms in an artery, it can cut off the supply of oxygen and nutrients to the tissues served by that artery, leading to damage or tissue death. If a thrombus forms in the heart, it can cause a heart attack. If a thrombus breaks off and travels through the bloodstream, it can lodge in a smaller vessel, causing blockage and potentially leading to damage in the organ that the vessel supplies. This is known as an embolism.

Thrombosis can occur due to various factors such as injury to the blood vessel wall, abnormalities in blood flow, or changes in the composition of the blood. Certain medical conditions, medications, and lifestyle factors can increase the risk of thrombosis. Treatment typically involves anticoagulant or thrombolytic therapy to dissolve or prevent further growth of the clot, as well as addressing any underlying causes.

Complement activating enzymes are proteins that play a crucial role in the activation of the complement system, which is a part of the immune system. The complement system is a complex series of biochemical reactions that help to eliminate pathogens and damaged cells from the body.

There are several types of complement activating enzymes, including:

1. Classical pathway activators: These include the C1, C4, and C2 components of the complement system. When activated, they trigger a series of reactions that lead to the formation of the membrane attack complex (MAC), which creates a pore in the membrane of the target cell, leading to its lysis.
2. Alternative pathway activators: These include factors B, D, and P. They are constantly active at low levels and can be activated by surfaces that are not normally found in the body, such as bacterial cell walls. Once activated, they also trigger the formation of the MAC.
3. Lectin pathway activators: These include mannose-binding lectin (MBL) and ficolins. They bind to carbohydrates on the surface of microbes and activate the complement system through the MBL-associated serine proteases (MASPs).

Overall, complement activating enzymes play a critical role in the immune response by helping to identify and eliminate pathogens and damaged cells from the body.

Cyclophosphamide is an alkylating agent, which is a type of chemotherapy medication. It works by interfering with the DNA of cancer cells, preventing them from dividing and growing. This helps to stop the spread of cancer in the body. Cyclophosphamide is used to treat various types of cancer, including lymphoma, leukemia, multiple myeloma, and breast cancer. It can be given orally as a tablet or intravenously as an injection.

Cyclophosphamide can also have immunosuppressive effects, which means it can suppress the activity of the immune system. This makes it useful in treating certain autoimmune diseases, such as rheumatoid arthritis and lupus. However, this immunosuppression can also increase the risk of infections and other side effects.

Like all chemotherapy medications, cyclophosphamide can cause a range of side effects, including nausea, vomiting, hair loss, fatigue, and increased susceptibility to infections. It is important for patients receiving cyclophosphamide to be closely monitored by their healthcare team to manage these side effects and ensure the medication is working effectively.

Mycophenolic Acid (MPA) is an immunosuppressive drug that is primarily used to prevent rejection in organ transplantation. It works by inhibiting the enzyme inosine monophosphate dehydrogenase, which is a key enzyme for the de novo synthesis of guanosine nucleotides, an essential component for the proliferation of T and B lymphocytes. By doing this, MPA reduces the activity of the immune system, thereby preventing it from attacking the transplanted organ.

Mycophenolic Acid is available in two forms: as the sodium salt (Mycophenolate Sodium) and as the morpholinoethyl ester (Mycophenolate Mofetil), which is rapidly hydrolyzed to Mycophenolic Acid after oral administration. Common side effects of MPA include gastrointestinal symptoms such as diarrhea, nausea, and vomiting, as well as an increased risk of infections due to its immunosuppressive effects.

OX40 ligand, also known as CD134L or TNFSF4, is a type II transmembrane protein belonging to the tumor necrosis factor (TNF) superfamily. It is a homotrimeric glycoprotein that plays an essential role in the activation and survival of T cells during immune responses.

The OX40 ligand binds to its receptor, OX40 (also known as CD134 or TNFRSF4), which is expressed on activated CD4+ and CD8+ T cells. The interaction between OX40L and OX40 provides a costimulatory signal that enhances T cell proliferation, survival, and effector functions.

OX40 ligand is primarily expressed on antigen-presenting cells such as dendritic cells, B cells, and macrophages, but it can also be induced on non-hematopoietic cells like endothelial cells and fibroblasts in response to inflammation.

In addition to its role in T cell activation, OX40 ligand has been implicated in the pathogenesis of various autoimmune diseases, making it a potential target for immunotherapy.

STAT4 (Signal Transducer and Activator of Transcription 4) is a transcription factor protein that plays a crucial role in the immune response. When activated, STAT4 translocates to the nucleus and binds to specific DNA sequences, regulating the expression of target genes involved in various cellular processes such as differentiation, proliferation, and activation of immune cells like T-cells.

Activation of STAT4 occurs through phosphorylation by receptor associated kinases, following cytokine stimulation, particularly interleukin (IL)-12 and type I interferons. Once activated, STAT4 forms homodimers or heterodimers with other STAT proteins, which then translocate to the nucleus and bind to specific DNA sequences called gamma-activated sites (GAS) in the promoter regions of target genes.

Mutations in the STAT4 gene have been associated with various autoimmune diseases, including rheumatoid arthritis, systemic lupus erythematosus, and multiple sclerosis, highlighting its importance in maintaining immune homeostasis.

Retrospective studies, also known as retrospective research or looking back studies, are a type of observational study that examines data from the past to draw conclusions about possible causal relationships between risk factors and outcomes. In these studies, researchers analyze existing records, medical charts, or previously collected data to test a hypothesis or answer a specific research question.

Retrospective studies can be useful for generating hypotheses and identifying trends, but they have limitations compared to prospective studies, which follow participants forward in time from exposure to outcome. Retrospective studies are subject to biases such as recall bias, selection bias, and information bias, which can affect the validity of the results. Therefore, retrospective studies should be interpreted with caution and used primarily to generate hypotheses for further testing in prospective studies.

Pregnancy complications refer to any health problems that arise during pregnancy which can put both the mother and the baby at risk. These complications may occur at any point during the pregnancy, from conception until childbirth. Some common pregnancy complications include:

1. Gestational diabetes: a type of diabetes that develops during pregnancy in women who did not have diabetes before becoming pregnant.
2. Preeclampsia: a pregnancy complication characterized by high blood pressure and damage to organs such as the liver or kidneys.
3. Placenta previa: a condition where the placenta covers the cervix, which can cause bleeding and may require delivery via cesarean section.
4. Preterm labor: when labor begins before 37 weeks of gestation, which can lead to premature birth and other complications.
5. Intrauterine growth restriction (IUGR): a condition where the fetus does not grow at a normal rate inside the womb.
6. Multiple pregnancies: carrying more than one baby, such as twins or triplets, which can increase the risk of premature labor and other complications.
7. Rh incompatibility: a condition where the mother's blood type is different from the baby's, which can cause anemia and jaundice in the newborn.
8. Pregnancy loss: including miscarriage, stillbirth, or ectopic pregnancy, which can be emotionally devastating for the parents.

It is important to monitor pregnancy closely and seek medical attention promptly if any concerning symptoms arise. With proper care and management, many pregnancy complications can be treated effectively, reducing the risk of harm to both the mother and the baby.

Monoclonal murine-derived antibodies are a type of laboratory-produced antibody that is identical in structure, having been derived from a single clone of cells. These antibodies are created using mouse cells and are therefore composed entirely of mouse immune proteins. They are designed to bind specifically to a particular target protein or antigen, making them useful tools for research, diagnostic testing, and therapeutic applications.

Monoclonal antibodies offer several advantages over polyclonal antibodies (which are derived from multiple clones of cells and can recognize multiple epitopes on an antigen). Monoclonal antibodies have a consistent and uniform structure, making them more reliable for research and diagnostic purposes. They also have higher specificity and affinity for their target antigens, allowing for more sensitive detection and measurement.

However, there are some limitations to using monoclonal murine-derived antibodies in therapeutic applications. Because they are composed entirely of mouse proteins, they can elicit an immune response in humans, leading to the production of human anti-mouse antibodies (HAMA) that can neutralize their effectiveness. To overcome this limitation, researchers have developed chimeric and humanized monoclonal antibodies that incorporate human protein sequences, reducing the risk of an immune response.

Kidney disease, also known as nephropathy or renal disease, refers to any functional or structural damage to the kidneys that impairs their ability to filter blood, regulate electrolytes, produce hormones, and maintain fluid balance. This damage can result from a wide range of causes, including diabetes, hypertension, glomerulonephritis, polycystic kidney disease, lupus, infections, drugs, toxins, and congenital or inherited disorders.

Depending on the severity and progression of the kidney damage, kidney diseases can be classified into two main categories: acute kidney injury (AKI) and chronic kidney disease (CKD). AKI is a sudden and often reversible loss of kidney function that occurs over hours to days, while CKD is a progressive and irreversible decline in kidney function that develops over months or years.

Symptoms of kidney diseases may include edema, proteinuria, hematuria, hypertension, electrolyte imbalances, metabolic acidosis, anemia, and decreased urine output. Treatment options depend on the underlying cause and severity of the disease and may include medications, dietary modifications, dialysis, or kidney transplantation.

Toll-like receptor 7 (TLR7) is a type of protein belonging to the family of Toll-like receptors, which are involved in the innate immune system's response to pathogens. TLR7 is primarily expressed on endosomal membranes of various immune cells, including dendritic cells, B cells, and macrophages. It recognizes single-stranded RNA molecules from viruses, thereby activating signaling pathways that lead to the production of proinflammatory cytokines and type I interferons. This response is crucial for initiating an effective immune response against viral infections.

Blood coagulation factors, also known as clotting factors, are a group of proteins that play a crucial role in the blood coagulation process. They are essential for maintaining hemostasis, which is the body's ability to stop bleeding after injury.

There are 13 known blood coagulation factors, and they are designated by Roman numerals I through XIII. These factors are produced in the liver and are normally present in an inactive form in the blood. When there is an injury to a blood vessel, the coagulation process is initiated, leading to the activation of these factors in a specific order.

The coagulation cascade involves two pathways: the intrinsic and extrinsic pathways. The intrinsic pathway is activated when there is damage to the blood vessel itself, while the extrinsic pathway is activated by tissue factor released from damaged tissues. Both pathways converge at the common pathway, leading to the formation of a fibrin clot.

Blood coagulation factors work together in a complex series of reactions that involve activation, binding, and proteolysis. When one factor is activated, it activates the next factor in the cascade, and so on. This process continues until a stable fibrin clot is formed.

Deficiencies or abnormalities in blood coagulation factors can lead to bleeding disorders such as hemophilia or thrombosis. Hemophilia is a genetic disorder that affects one or more of the coagulation factors, leading to excessive bleeding and difficulty forming clots. Thrombosis, on the other hand, occurs when there is an abnormal formation of blood clots in the blood vessels, which can lead to serious complications such as stroke or pulmonary embolism.

Protein-losing enteropathies (PLE) refer to a group of conditions characterized by excessive loss of proteins from the gastrointestinal tract into the intestinal lumen and ultimately into the stool. This results in hypoproteinemia, which is a decrease in the concentration of proteins in the bloodstream, particularly albumin.

The protein loss can occur due to various reasons such as increased permeability of the intestinal mucosa, lymphatic obstruction, or inflammatory processes affecting the gastrointestinal tract. Common causes of PLE include conditions such as inflammatory bowel disease, intestinal lymphangiectasia, celiac disease, Whipple's disease, and menetrier's disease.

Symptoms of PLE may include edema, ascites, weight loss, diarrhea, and fatigue. The diagnosis of PLE typically involves measuring the concentration of proteins in the stool, as well as other diagnostic tests to determine the underlying cause. Treatment of PLE depends on the underlying cause and may involve dietary modifications, medications, or surgical interventions.

Central nervous system (CNS) diseases refer to medical conditions that primarily affect the brain and spinal cord. The CNS is responsible for controlling various functions in the body, including movement, sensation, cognition, and behavior. Therefore, diseases of the CNS can have significant impacts on a person's quality of life and overall health.

There are many different types of CNS diseases, including:

1. Infectious diseases: These are caused by viruses, bacteria, fungi, or parasites that infect the brain or spinal cord. Examples include meningitis, encephalitis, and polio.
2. Neurodegenerative diseases: These are characterized by progressive loss of nerve cells in the brain or spinal cord. Examples include Alzheimer's disease, Parkinson's disease, and Huntington's disease.
3. Structural diseases: These involve damage to the physical structure of the brain or spinal cord, such as from trauma, tumors, or stroke.
4. Functional diseases: These affect the function of the nervous system without obvious structural damage, such as multiple sclerosis and epilepsy.
5. Genetic disorders: Some CNS diseases are caused by genetic mutations, such as spinal muscular atrophy and Friedreich's ataxia.

Symptoms of CNS diseases can vary widely depending on the specific condition and the area of the brain or spinal cord that is affected. They may include muscle weakness, paralysis, seizures, loss of sensation, difficulty with coordination and balance, confusion, memory loss, changes in behavior or mood, and pain. Treatment for CNS diseases depends on the specific condition and may involve medications, surgery, rehabilitation therapy, or a combination of these approaches.

Antirheumatic agents are a class of drugs used to treat rheumatoid arthritis, other inflammatory types of arthritis, and related conditions. These medications work by reducing inflammation in the body, relieving symptoms such as pain, swelling, and stiffness in the joints. They can also help slow down or prevent joint damage and disability caused by the disease.

There are several types of antirheumatic agents, including:

1. Nonsteroidal anti-inflammatory drugs (NSAIDs): These medications, such as ibuprofen and naproxen, reduce inflammation and relieve pain. They are often used to treat mild to moderate symptoms of arthritis.
2. Corticosteroids: These powerful anti-inflammatory drugs, such as prednisone and cortisone, can quickly reduce inflammation and suppress the immune system. They are usually used for short-term relief of severe symptoms or in combination with other antirheumatic agents.
3. Disease-modifying antirheumatic drugs (DMARDs): These medications, such as methotrexate and hydroxychloroquine, work by slowing down the progression of rheumatoid arthritis and preventing joint damage. They can take several weeks or months to become fully effective.
4. Biologic response modifiers (biologics): These are a newer class of DMARDs that target specific molecules involved in the immune response. They include drugs such as adalimumab, etanercept, and infliximab. Biologics are usually used in combination with other antirheumatic agents for patients who have not responded to traditional DMARD therapy.
5. Janus kinase (JAK) inhibitors: These medications, such as tofacitinib and baricitinib, work by blocking the action of enzymes called JAKs that are involved in the immune response. They are used to treat moderate to severe rheumatoid arthritis and can be used in combination with other antirheumatic agents.

It is important to note that antirheumatic agents can have significant side effects and should only be prescribed by a healthcare provider who is experienced in the management of rheumatoid arthritis. Regular monitoring and follow-up are essential to ensure safe and effective treatment.

Toll-like receptor 9 (TLR9) is a type of protein belonging to the family of Toll-like receptors, which play a crucial role in the innate immune system. TLR9 is primarily expressed on the endosomal membranes of various immune cells, including dendritic cells, B cells, and macrophages. It recognizes specific molecular patterns, particularly unmethylated CpG DNA motifs, which are commonly found in bacterial and viral genomes but are underrepresented in vertebrate DNA.

Upon recognition and binding to its ligands, TLR9 initiates a signaling cascade that activates various transcription factors, such as NF-κB and IRF7, leading to the production of proinflammatory cytokines, type I interferons, and the activation of adaptive immune responses. This process is essential for the clearance of pathogens and the development of immunity against them. Dysregulation of TLR9 signaling has been implicated in several autoimmune diseases and chronic inflammatory conditions.

The term "Asian Continental Ancestry Group" is a medical/ethnic classification used to describe a person's genetic background and ancestry. According to this categorization, individuals with origins in the Asian continent are grouped together. This includes populations from regions such as East Asia (e.g., China, Japan, Korea), South Asia (e.g., India, Pakistan, Bangladesh), Southeast Asia (e.g., Philippines, Indonesia, Thailand), and Central Asia (e.g., Kazakhstan, Uzbekistan, Tajikistan). It is important to note that this broad categorization may not fully capture the genetic diversity within these regions or accurately reflect an individual's specific ancestral origins.

Raynaud's disease, also known as Raynaud's phenomenon or syndrome, is a condition that affects the blood vessels, particularly in the fingers and toes. It is characterized by episodes of vasospasm (constriction) of the small digital arteries and arterioles, which can be triggered by cold temperatures or emotional stress. This results in reduced blood flow to the affected areas, causing them to become pale or white and then cyanotic (blue) due to the accumulation of deoxygenated blood. As the episode resolves, the affected areas may turn red as blood flow returns, sometimes accompanied by pain, numbness, or tingling sensations.

Raynaud's disease can be primary, meaning it occurs without an underlying medical condition, or secondary, which is associated with connective tissue disorders, autoimmune diseases, or other health issues such as carpal tunnel syndrome, vibration tool usage, or smoking. Primary Raynaud's is more common and tends to be less severe than secondary Raynaud's.

Treatment for Raynaud's disease typically involves avoiding triggers, keeping the body warm, and using medications to help dilate blood vessels and improve circulation. In some cases, lifestyle modifications and smoking cessation may also be recommended to manage symptoms and prevent progression of the condition.

"Cells, cultured" is a medical term that refers to cells that have been removed from an organism and grown in controlled laboratory conditions outside of the body. This process is called cell culture and it allows scientists to study cells in a more controlled and accessible environment than they would have inside the body. Cultured cells can be derived from a variety of sources, including tissues, organs, or fluids from humans, animals, or cell lines that have been previously established in the laboratory.

Cell culture involves several steps, including isolation of the cells from the tissue, purification and characterization of the cells, and maintenance of the cells in appropriate growth conditions. The cells are typically grown in specialized media that contain nutrients, growth factors, and other components necessary for their survival and proliferation. Cultured cells can be used for a variety of purposes, including basic research, drug development and testing, and production of biological products such as vaccines and gene therapies.

It is important to note that cultured cells may behave differently than they do in the body, and results obtained from cell culture studies may not always translate directly to human physiology or disease. Therefore, it is essential to validate findings from cell culture experiments using additional models and ultimately in clinical trials involving human subjects.

Disease progression is the worsening or advancement of a medical condition over time. It refers to the natural course of a disease, including its development, the severity of symptoms and complications, and the impact on the patient's overall health and quality of life. Understanding disease progression is important for developing appropriate treatment plans, monitoring response to therapy, and predicting outcomes.

The rate of disease progression can vary widely depending on the type of medical condition, individual patient factors, and the effectiveness of treatment. Some diseases may progress rapidly over a short period of time, while others may progress more slowly over many years. In some cases, disease progression may be slowed or even halted with appropriate medical interventions, while in other cases, the progression may be inevitable and irreversible.

In clinical practice, healthcare providers closely monitor disease progression through regular assessments, imaging studies, and laboratory tests. This information is used to guide treatment decisions and adjust care plans as needed to optimize patient outcomes and improve quality of life.

Congenic mice are strains that have been developed through a specific breeding process to be genetically identical, except for a small region of interest (ROI) that has been introgressed from a donor strain. This is achieved by repeatedly backcrossing the donor ROI onto the genetic background of a recipient strain for many generations, followed by intercrossing within the resulting congenic line to ensure homozygosity of the ROI.

The goal of creating congenic mice is to study the effects of a specific gene or genomic region while minimizing the influence of other genetic differences between strains. This allows researchers to investigate the relationship between genotype and phenotype more accurately, which can be particularly useful in biomedical research for understanding complex traits, diseases, and potential therapeutic targets.

Interferon type I is a class of signaling proteins, also known as cytokines, that are produced and released by cells in response to the presence of pathogens such as viruses, bacteria, and parasites. These interferons play a crucial role in the body's innate immune system and help to establish an antiviral state in surrounding cells to prevent the spread of infection.

Interferon type I includes several subtypes, such as interferon-alpha (IFN-α), interferon-beta (IFN-β), and interferon-omega (IFN-ω). When produced, these interferons bind to specific receptors on the surface of nearby cells, triggering a cascade of intracellular signaling events that lead to the activation of genes involved in the antiviral response.

The activation of these genes results in the production of enzymes that inhibit viral replication and promote the destruction of infected cells. Interferon type I also enhances the adaptive immune response by promoting the activation and proliferation of immune cells such as T-cells and natural killer (NK) cells, which can directly target and eliminate infected cells.

Overall, interferon type I plays a critical role in the body's defense against viral infections and is an important component of the immune response to many different types of pathogens.

Prospective studies, also known as longitudinal studies, are a type of cohort study in which data is collected forward in time, following a group of individuals who share a common characteristic or exposure over a period of time. The researchers clearly define the study population and exposure of interest at the beginning of the study and follow up with the participants to determine the outcomes that develop over time. This type of study design allows for the investigation of causal relationships between exposures and outcomes, as well as the identification of risk factors and the estimation of disease incidence rates. Prospective studies are particularly useful in epidemiology and medical research when studying diseases with long latency periods or rare outcomes.

An oral ulcer is a defect or break in the continuity of the epithelium, the tissue that lines the inner surface of the mouth, leading to an inflamed, painful, and sometimes bleeding lesion. They can be classified as primary (e.g., aphthous ulcers, traumatic ulcers) or secondary (e.g., those caused by infections, underlying systemic conditions, or reactions to medications). Oral ulcers may cause discomfort, impacting speech and food consumption, and their presence might indicate an underlying medical issue that requires further evaluation.

A Complement Hemolytic Activity Assay is a laboratory test used to measure the functionality and activity level of the complement system, which is a part of the immune system. The complement system is a group of proteins that work together to help eliminate pathogens from the body.

The assay measures the ability of the complement system to lyse (break open) red blood cells. This is done by mixing the patient's serum (the liquid portion of the blood) with antibody-coated red blood cells and incubating them together. The complement proteins in the serum will then bind to the antibodies on the red blood cells and cause them to lyse.

The degree of hemolysis (red blood cell lysis) is directly proportional to the activity level of the complement system. By measuring the amount of hemolysis, the assay can determine whether the complement system is functioning properly and at what level of activity.

This test is often used to diagnose or monitor complement-mediated diseases such as autoimmune disorders, infections, and some types of cancer. It may also be used to evaluate the effectiveness of treatments that target the complement system.

The "age of onset" is a medical term that refers to the age at which an individual first develops or displays symptoms of a particular disease, disorder, or condition. It can be used to describe various medical conditions, including both physical and mental health disorders. The age of onset can have implications for prognosis, treatment approaches, and potential causes of the condition. In some cases, early onset may indicate a more severe or progressive course of the disease, while late-onset symptoms might be associated with different underlying factors or etiologies. It is essential to provide accurate and precise information regarding the age of onset when discussing a patient's medical history and treatment plan.

Follow-up studies are a type of longitudinal research that involve repeated observations or measurements of the same variables over a period of time, in order to understand their long-term effects or outcomes. In medical context, follow-up studies are often used to evaluate the safety and efficacy of medical treatments, interventions, or procedures.

In a typical follow-up study, a group of individuals (called a cohort) who have received a particular treatment or intervention are identified and then followed over time through periodic assessments or data collection. The data collected may include information on clinical outcomes, adverse events, changes in symptoms or functional status, and other relevant measures.

The results of follow-up studies can provide important insights into the long-term benefits and risks of medical interventions, as well as help to identify factors that may influence treatment effectiveness or patient outcomes. However, it is important to note that follow-up studies can be subject to various biases and limitations, such as loss to follow-up, recall bias, and changes in clinical practice over time, which must be carefully considered when interpreting the results.

Complement receptors are proteins found on the surface of various cells in the human body, including immune cells and some non-immune cells. They play a crucial role in the complement system, which is a part of the innate immune response that helps to eliminate pathogens and damaged cells from the body. Complement receptors bind to complement proteins or fragments that are generated during the activation of the complement system. This binding triggers various intracellular signaling events that can lead to diverse cellular responses, such as phagocytosis, inflammation, and immune regulation.

There are several types of complement receptors, including:

1. CR1 (CD35): A receptor found on erythrocytes, B cells, neutrophils, monocytes, macrophages, and glomerular podocytes. It functions in the clearance of immune complexes and regulates complement activation.
2. CR2 (CD21): Expressed mainly on B cells and follicular dendritic cells. It facilitates antigen presentation, B-cell activation, and immune regulation.
3. CR3 (CD11b/CD18, Mac-1): Present on neutrophils, monocytes, macrophages, and some T cells. It mediates cell adhesion, phagocytosis, and intracellular signaling.
4. CR4 (CD11c/CD18, p150,95): Expressed on neutrophils, monocytes, macrophages, and dendritic cells. It is involved in cell adhesion, phagocytosis, and intracellular signaling.
5. C5aR (CD88): Found on various immune cells, including neutrophils, monocytes, macrophages, mast cells, eosinophils, and dendritic cells. It binds to the complement protein C5a and mediates chemotaxis, degranulation, and inflammation.
6. C5L2 (GPR77): Present on various cell types, including immune cells. Its function is not well understood but may involve regulating C5a-mediated responses or acting as a receptor for other ligands.

These receptors play crucial roles in the immune response and inflammation by mediating various functions such as chemotaxis, phagocytosis, cell adhesion, and intracellular signaling. Dysregulation of these receptors has been implicated in several diseases, including autoimmune disorders, infections, and cancer.

Protein Tyrosine Phosphatase, Non-Receptor Type 22 (PTPN22) is a gene that encodes a protein tyrosine phosphatase, which is an enzyme that regulates various cellular processes by removing phosphate groups from tyrosine residues on proteins. This particular phosphatase is a non-receptor type, meaning it does not have a transmembrane domain and is found in the cytoplasm.

The PTPN22 protein plays a crucial role in regulating immune cell function, particularly T cells, by modulating signaling pathways that are important for their activation and differentiation. Variations in the PTPN22 gene have been associated with an increased risk of developing several autoimmune diseases, including rheumatoid arthritis, type 1 diabetes, and systemic lupus erythematosus. These genetic variations may lead to altered enzymatic activity or expression levels of the PTPN22 protein, resulting in dysregulated immune responses and increased susceptibility to autoimmune diseases.

Facial dermatoses refer to various skin conditions that affect the face. These can include a wide range of disorders, such as:

1. Acne vulgaris: A common skin condition characterized by the formation of comedones (blackheads and whiteheads) and inflammatory papules, pustules, and nodules. It primarily affects the face, neck, chest, and back.
2. Rosacea: A chronic skin condition that causes redness, flushing, and visible blood vessels on the face, along with bumps or pimples and sometimes eye irritation.
3. Seborrheic dermatitis: A common inflammatory skin disorder that causes a red, itchy, and flaky rash, often on the scalp, face, and eyebrows. It can also affect other oily areas of the body, like the sides of the nose and behind the ears.
4. Atopic dermatitis (eczema): A chronic inflammatory skin condition that causes red, itchy, and scaly patches on the skin. While it can occur anywhere on the body, it frequently affects the face, especially in infants and young children.
5. Psoriasis: An autoimmune disorder that results in thick, scaly, silvery, or red patches on the skin. It can affect any part of the body, including the face.
6. Contact dermatitis: A skin reaction caused by direct contact with an allergen or irritant, resulting in redness, itching, and inflammation. The face can be affected when allergens or irritants come into contact with the skin through cosmetics, skincare products, or other substances.
7. Lupus erythematosus: An autoimmune disorder that can cause a butterfly-shaped rash on the cheeks and nose, along with other symptoms like joint pain, fatigue, and photosensitivity.
8. Perioral dermatitis: A inflammatory skin condition that causes redness, small bumps, and dryness around the mouth, often mistaken for acne. It can also affect the skin around the nose and eyes.
9. Vitiligo: An autoimmune disorder that results in the loss of pigmentation in patches of skin, which can occur on the face and other parts of the body.
10. Tinea faciei: A fungal infection that affects the facial skin, causing red, scaly, or itchy patches. It is also known as ringworm of the face.

These are just a few examples of skin conditions that can affect the face. If you experience any unusual symptoms or changes in your skin, it's essential to consult a dermatologist for proper diagnosis and treatment.

Anti-inflammatory agents are a class of drugs or substances that reduce inflammation in the body. They work by inhibiting the production of inflammatory mediators, such as prostaglandins and leukotrienes, which are released during an immune response and contribute to symptoms like pain, swelling, redness, and warmth.

There are two main types of anti-inflammatory agents: steroidal and nonsteroidal. Steroidal anti-inflammatory drugs (SAIDs) include corticosteroids, which mimic the effects of hormones produced by the adrenal gland. Nonsteroidal anti-inflammatory drugs (NSAIDs) are a larger group that includes both prescription and over-the-counter medications, such as aspirin, ibuprofen, naproxen, and celecoxib.

While both types of anti-inflammatory agents can be effective in reducing inflammation and relieving symptoms, they differ in their mechanisms of action, side effects, and potential risks. Long-term use of NSAIDs, for example, can increase the risk of gastrointestinal bleeding, kidney damage, and cardiovascular events. Corticosteroids can have significant side effects as well, particularly with long-term use, including weight gain, mood changes, and increased susceptibility to infections.

It's important to use anti-inflammatory agents only as directed by a healthcare provider, and to be aware of potential risks and interactions with other medications or health conditions.

Immunologic factors refer to the elements of the immune system that contribute to the body's defense against foreign substances, infectious agents, and cancerous cells. These factors include various types of white blood cells (such as lymphocytes, neutrophils, monocytes, and eosinophils), antibodies, complement proteins, cytokines, and other molecules involved in the immune response.

Immunologic factors can be categorized into two main types: innate immunity and adaptive immunity. Innate immunity is the non-specific defense mechanism that provides immediate protection against pathogens through physical barriers (e.g., skin, mucous membranes), chemical barriers (e.g., stomach acid, enzymes), and inflammatory responses. Adaptive immunity, on the other hand, is a specific defense mechanism that develops over time as the immune system learns to recognize and respond to particular pathogens or antigens.

Abnormalities in immunologic factors can lead to various medical conditions, such as autoimmune disorders, immunodeficiency diseases, and allergies. Therefore, understanding immunologic factors is crucial for diagnosing and treating these conditions.

Complement activation is the process by which the complement system, a part of the immune system, is activated to help eliminate pathogens and damaged cells from the body. The complement system consists of a group of proteins that work together to recognize and destroy foreign substances.

Activation of the complement system can occur through three different pathways: the classical pathway, the lectin pathway, and the alternative pathway. Each pathway involves a series of proteolytic reactions that ultimately result in the formation of the membrane attack complex (MAC), which creates a pore in the membrane of the target cell, leading to its lysis and removal.

The classical pathway is typically activated by the binding of antibodies to antigens on the surface of a pathogen or damaged cell. The lectin pathway is activated by the recognition of specific carbohydrate structures on the surface of microorganisms. The alternative pathway can be spontaneously activated and serves as an amplification loop for both the classical and lectin pathways.

Complement activation plays a crucial role in the immune response, but uncontrolled or excessive activation can also lead to tissue damage and inflammation. Dysregulation of complement activation has been implicated in various diseases, including autoimmune disorders, inflammatory conditions, and neurodegenerative diseases.

HLA-DR3 antigen is a type of human leukocyte antigen (HLA) class II histocompatibility antigen. HLAs are proteins found on the surface of cells that help the immune system distinguish between the body's own cells and foreign substances. The HLA-DR3 antigen is encoded by the DRB1*03:01 gene and is commonly found in individuals with certain autoimmune diseases, such as rheumatoid arthritis, type 1 diabetes, and celiac disease.

The HLA-DR3 antigen plays a role in presenting pieces of proteins (peptides) to CD4+ T cells, which are a type of white blood cell that helps coordinate the immune response. The presentation of specific peptides by the HLA-DR3 antigen can lead to an abnormal immune response in some individuals, resulting in the development of autoimmune diseases.

It's important to note that having the HLA-DR3 antigen does not guarantee that a person will develop an autoimmune disease, as other genetic and environmental factors also play a role.

African Americans are defined as individuals who have ancestry from any of the black racial groups of Africa. This term is often used to describe people living in the United States who have total or partial descent from enslaved African peoples. The term does not refer to a single ethnicity but is a broad term that includes various ethnic groups with diverse cultures, languages, and traditions. It's important to note that some individuals may prefer to identify as Black or of African descent rather than African American, depending on their personal identity and background.

An epitope is a specific region on the surface of an antigen (a molecule that can trigger an immune response) that is recognized by an antibody, B-cell receptor, or T-cell receptor. It is also commonly referred to as an antigenic determinant. Epitopes are typically composed of linear amino acid sequences or conformational structures made up of discontinuous amino acids in the antigen. They play a crucial role in the immune system's ability to differentiate between self and non-self molecules, leading to the targeted destruction of foreign substances like viruses and bacteria. Understanding epitopes is essential for developing vaccines, diagnostic tests, and immunotherapies.

Histiocytic Necrotizing Lymphadenitis is a condition characterized by the inflammation and necrosis (death of tissue) of lymph nodes, caused by an abnormal proliferation and activation of histiocytes (a type of white blood cell). It is also known as Kikuchi's disease. The exact cause of this condition is unknown, but it is thought to be related to an immune response to viral infections or other antigens.

Histopathologically, it is characterized by the presence of necrotizing granulomatous inflammation with histiocytic predominance and absence of neutrophils. The condition is typically self-limiting, with symptoms resolving within a few months without specific treatment. However, in some cases, it can be associated with systemic symptoms or other autoimmune disorders.

In medical terms, the skin is the largest organ of the human body. It consists of two main layers: the epidermis (outer layer) and dermis (inner layer), as well as accessory structures like hair follicles, sweat glands, and oil glands. The skin plays a crucial role in protecting us from external factors such as bacteria, viruses, and environmental hazards, while also regulating body temperature and enabling the sense of touch.

Treatment outcome is a term used to describe the result or effect of medical treatment on a patient's health status. It can be measured in various ways, such as through symptoms improvement, disease remission, reduced disability, improved quality of life, or survival rates. The treatment outcome helps healthcare providers evaluate the effectiveness of a particular treatment plan and make informed decisions about future care. It is also used in clinical research to compare the efficacy of different treatments and improve patient care.

... systemic lupus erythematosus or NPSLE refers to the neurological and psychiatric manifestations of systemic lupus erythematosus ... 2010). "EULAR recommendations for the management of systemic lupus erythematosus with neuropsychiatric manifestations: report ... "Neuropsychiatric Syndromes in Systemic Lupus Erythematosus: A Meta-Analysis". Seminars in Arthritis and Rheumatism. 41 (1): 1- ... "Management of Neuropsychiatric Systemic Lupus Erythematosus: Current Approaches and Future Perspectives". Drugs. 76 (4): 459- ...
While these symptoms are similar to those of systemic lupus erythematosus, they are generally not as severe unless they are ... Anti-histone antibody Lupus erythematosus Hydralazine Discoid lupus erythematosus List of cutaneous conditions Rubin, Robert L ... ISBN 978-0-8089-1543-0. Lahita, Robert G. (1987). Systemic Lupus Erythematosus. New York: John Wiley & Sons. p. 859. ISBN 978-0 ... July 1983). The Clinical Management of Systemic Lupus Erythematosus. New York: Grune & Stratton. p. 221. ...
... drug-induced lupus erythematosus neonatal lupus erythematosus systemic lupus erythematosus There is still no cure for lupus but ... lupus erythematosus profundus) tumid lupus erythematosus verrucous lupus erythematosus (hypertrophic lupus erythematosus) ... lupus erythematosus generalized discoid lupus erythematosus localized discoid lupus erythematosus chilblain lupus erythematosus ... 70% of lupus cases diagnosed are systemic lupus erythematosus. 20% of people with lupus will have a parent or sibling who ...
"Cutaneous lupus erythematosus: diagnosis and treatment". Best Practice & Research. Clinical Rheumatology. Systemic Lupus ... Cutaneous lupus erythematosus is associated with both lupus erythematosus-specific lesions and cutaneous manifestations that ... Because of the diagnostic criteria used to diagnose systemic lupus erythematosus, a patient with only cutaneous manifestations ... Acute cutaneous lupus erythematosus can be either localized or generalized. The localized form of the disease is most commonly ...
Wikimedia Commons has media related to Systemic lupus erythematosus. Lupus at Curlie Systemic Lupus Erythematosus at the ... There are a number of other kinds of lupus erythematosus including discoid lupus erythematosus, neonatal lupus, and subacute ... Lupus Erythematosus: A review of the current status of Discoid and Systemic Lupus Erythematosus. New York: McGraw Hill. pp. 1-9 ... Lupus, technically known as systemic lupus erythematosus (SLE), is an autoimmune disease in which the body's immune system ...
... is an inflammation of the kidneys caused by systemic lupus erythematosus (SLE), an autoimmune disease. It is a ... Karageorgas TP, Tseronis DD, Mavragani CP (2011). "Activation of type I interferon pathway in systemic lupus erythematosus: ... February 2004). "The classification of glomerulonephritis in systemic lupus erythematosus revisited". J. Am. Soc. Nephrol. 15 ( ... Lahita, Robert G. (2004-06-09). Systemic Lupus Erythematosus. Academic Press. ISBN 9780080474540. Greenberg, Arthur; Cheung, ...
Papadimitraki ED, Bertsias G, Chamilos G, Boumpas DT (January 2011). "Systemic Lupus Erythematosus". Academic Press. pp. 1083- ...
Phang KF, Cho J, Lee W, Mak A (2018). "Glucocorticoid-induced osteoporosis in systemic lupus erythematosus". Rheumatology ... Methylprednisolone is used to treat several rheumatic diseases, such as Systemic Lupus Erythematosus (SLE) and Rheumatoid ... "Systemic lupus erythematosus". Nat Rev Dis Primers. 2: 16039. doi:10.1038/nrdp.2016.39. PMID 27306639. S2CID 2628865. Chan TM ( ... systemic lupus erythematosus, acute and subacute bursitis, synovitis of osteoarthritis, post-traumatic osteoarthritis, and ...
ISBN 0-7216-2921-0. "Systemic Lupus Erythematosus". The Lecturio Medical Concept Library. Retrieved 22 August 2021. Wollenhaupt ... Familial Mediterranean fever Systemic lupus erythematosus An undifferentiated arthritis is an arthritis that does not fit into ... Lupus is a common collagen vascular disorder that can be present with severe arthritis. Other features of lupus include a skin ... Other types include gout, lupus, fibromyalgia, and septic arthritis. They are all types of rheumatic disease. Treatment may ...
Estes, Dorothy; Christian, Charles L. (1971). "The Natural History of Systemic Lupus Erythematosus by Prospective Analysis". ... Tsokos, George C. (2011). "Systemic Lupus Erythematosus". New England Journal of Medicine. 365 (22): 2110-21. doi:10.1056/ ... may be a forme fruste of systemic lupus erythematosus (SLE) associated optic neuropathy. AON is more than the presence of any ... "Optic Neuropathy and Chiasmopathy in the Diagnosis of Systemic Lupus Erythematosus". Journal of Neuro-Ophthalmology. 21 (3): ...
Deng Y, Hahn BH, Tsao BP (2013). "Systemic Lupus Erythematosus". Emery and Rimoin's Principles and Practice of Medical Genetics ...
Systemic lupus erythematosus. The Systemic Lupus Erythematosus Quality of Life measure (L-QoL or SLEQoL) was published in 2009 ... Systemic Lupus Erythematosus-Specific Quality of Life Questionnaire (SLEQOL), and Systemic Lupus Erythematosus Quality of Life ... Yazdany J (November 2011). "Health-related quality of life measurement in adult systemic lupus erythematosus: Lupus Quality of ... a quality-of-life instrument specific to systemic lupus erythematosus". Annals of the Rheumatic Diseases. 68 (2): 196-200. doi: ...
cite book}}: ,journal= ignored (help) Jones JM, Martinez AJ, Joshi VV, McWilliams N (March 1975). "Systemic lupus erythematosus ... These, or similar, bodies have been found increased in the presence of lymphoid cancers and SLE (lupus). They are also observed ...
... such as systemic lupus erythematosus or scleroderma. Latent lupus and incomplete lupus are alternative terms that have been ... such as systemic lupus erythematosus (SLE); systemic sclerosis (SSc); dermatomyositis (DM); polymyositis (PM); anti-synthetase ... It can occur alone or with rheumatoid arthritis, scleroderma, or systemic lupus erythematosus. Nine out of 10 cases occur in ... "Systemic lupus erythematosus". Genetics Home Reference. Retrieved 2019-11-19. Reference, Genetics Home. "Rheumatoid arthritis ...
Systemic lupus erythematosus (SLE), referred to simply as lupus, is a systemic autoimmune disease that affects multiple organs ... For example, antinuclear antibody (ANA) testing is commonly used in the diagnosis of systemic lupus erythematosus (SLE) and ... Tsokos GC (December 2011). "Systemic lupus erythematosus". The New England Journal of Medicine. 365 (22): 2110-21. doi:10.1056/ ... and systemic lupus erythematosus. Diagnosing autoimmune diseases can be challenging due to their diverse presentations and the ...
D'Cruz, David P; Khamashta, Munther A; Hughes, Graham RV (2007). "Systemic lupus erythematosus". The Lancet. Elsevier BV. 369 ( ... Autoimmune disease: Diseases like lupus can cause visible skin rashes or facial flushing. Alopecia areata: Leads to hair loss, ...
... and pancreatic disorders in systemic lupus erythematosus.". Systemic Lupus Erythematosus. Academic Press. pp. 391-401. doi: ... and Pancreatic Disorders in Systemic Lupus Erythematosus", Systemic Lupus Erythematosus, Elsevier, pp. 391-401 Gosemann JH, ...
García-Carrasco M, Pinto CM, Poblano JC, Morales IE, Cervera R, Anaya JM (2013-07-18). "Systemic lupus erythematosus". In Anaya ... Thrombolysis can be systemic via IV alteplase (tPA) or catheter-directed. tPA works to break up the clot. A major risk of tPA ...
"Systemic Lupus Erythematosus. Lupus treatment; information , Patient". Patient. Retrieved 21 September 2016. " ... Systemic lupus erythematosus is associated with low C3 and C4. Membranoproliferative glomerulonephritis usually has low C3. The ... C4: C4 deficiency is highly associated with systemic lupus erythematosus. Aβ42, a protein involved in Alzheimer's disease, can ...
In systemic lupus erythematosus, the Zap-70 receptor pathway is missing and the homolog Syk takes its place. ZAP-70 deficiency ... Tsokos GC (December 2011). "Systemic lupus erythematosus". The New England Journal of Medicine. 365 (22): 2110-21. doi:10.1056/ ...
Lahita is the editor of the standard textbook Systemic Lupus Erythematosus (5th edition), now Lahita's Systemic Lupus ... "Systemic Lupus Erythematosus - 4th Edition". www.elsevier.com. Retrieved 2018-08-20. "Why The Body Attacks Itself". Retrieved ... Neuropsychiatric Manifestations of Systemic Lupus Erythematosus. Annals of the New York Academy of Sciences, 1999. Lahita, ... Novel Treatments for Systemic Lupus Erythematosus. Vol 3, no 5, pp255-266. Therapeutic Advances in Musculoskeletal Disease. ...
... systemic lupus erythematosus (SLE), scleroderma (systemic sclerosis or SSc), and pemphigus vulgaris (PV) with success for some ... D'Cruz DP, Khamashta MA, Hughes GR (February 2007). "Systemic lupus erythematosus". Lancet. 369 (9561): 587-96. CiteSeerX 10.1. ... Walsh proposed that mycophenolate should be considered as a first-line induction therapy for treatment of lupus nephritis in ... Its increasing application in treating lupus nephritis has demonstrated more frequent complete response and less frequent ...
This is particularly noteworthy because systemic lupus erythematosus, a canonical type III hypersensitivity-driven autoimmune ... "Systemic lupus erythematosus". Nature Reviews Disease Primers. 2 (1): 1-21. doi:10.1038/nrdp.2016.39. ISSN 2056-676X. Ravetch, ...
"Systemic Lupus Erythematosus". PracticeUpdate. 26 February 2021. "Lee Goldman, MD - Taiwan Society of Internal Medicine". ...
Hill, L. C. (1957). "Systemic Lupus Erythematosus". BMJ. 2 (5046): 655-660 contd. doi:10.1136/bmj.2.5046.655. PMC 1962315. PMID ... Systemic Lupus Erythematosus 1958 John St. Clair Elkington, Cerebral Vascular Disease in the light of Modern Techniques 1959 ...
Anti-β2-GP1 antibodies are found in both infectious and some systemic autoimmune diseases (eg. systemic lupus erythematosus ( ... Anti-β2-GP1 antibodies are strongly associated with thrombotic forms of lupus. In molecular biology, the protein domain Sushi 2 ... Lupus. 1 (2): 75-81. doi:10.1177/096120339200100204. PMID 1301967. S2CID 35296154. Shi T, Giannakopoulos B, Iverson GM, ... "Beta2-glycoprotein I dependent anticardiolipin antibodies and lupus anticoagulant in patients with recurrent pregnancy loss". ...
Systemic lupus erythematosus (SLE). Ménétrier's disease. Zollinger-Ellison syndrome. Eosinophilic gastroenteritis. Coeliac ... Swelling of the legs due to peripheral edema can also occur, however, if the PLE is related to a systemic disease such as ...
... from other headache types in people with lupus. Cuadrado MJ, Sanna G (2003). "Headache and systemic lupus erythematosus". Lupus ... "Lupus headaches in childhood-onset systemic lupus erythematosus: relationship to disease activity as measured by the systemic ... Lupus headache is an important item in the Systemic Lupus Erythematosus Disease Activity Index (SLEDAI), a scoring system often ... Lupus headache is a proposed, specific headache disorder in patients with systemic lupus erythematosus (SLE). Research shows ...
Autoimmune diseases Systemic lupus erythematosus. Cancer-caused aseptic meningitis such as neoplastic meningitis This affects ...
"Skin inflammatory (nontumor) > Lichenoid and interface reaction patterns > Lupus: systemic lupus erythematosus (SLE)". ... lupus erythematosus and dermatomyositis. Bolognia, Jean L.; et al. (2007). Dermatology. St. Louis: Mosby. p. 11. ISBN 1-4160- ...
... is the most common type of lupus. SLE is an autoimmune disease in which the immune system attacks its own tissues, causing ... Systemic lupus erythematosus (SLE), is the most common type of lupus. SLE is an autoimmune disease in which the immune system ... Lupus QoL-US benchmarks for US patients with systemic lupus erythematosus. J Rheumatol. 2010;37(9):1828-1833. doi:10.3899/ ... The incidence and prevalence of systemic lupus erythematosus in New York County (Manhattan), New York: The Manhattan Lupus ...
... systemic lupus erythematosus or NPSLE refers to the neurological and psychiatric manifestations of systemic lupus erythematosus ... 2010). "EULAR recommendations for the management of systemic lupus erythematosus with neuropsychiatric manifestations: report ... "Neuropsychiatric Syndromes in Systemic Lupus Erythematosus: A Meta-Analysis". Seminars in Arthritis and Rheumatism. 41 (1): 1- ... "Management of Neuropsychiatric Systemic Lupus Erythematosus: Current Approaches and Future Perspectives". Drugs. 76 (4): 459- ...
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Systemic lupus erythematosus (SLE) is an autoimmune disease. In this disease, the immune system of the body mistakenly attacks ... Systemic lupus erythematosus (SLE) is an autoimmune disease. In this disease, the immune system of the body mistakenly attacks ... Disseminated lupus erythematosus; SLE; Lupus; Lupus erythematosus; Butterfly rash - SLE; Discoid lupus ... Systemic lupus erythematosus (SLE) is an autoimmune disease. In this disease, the immune system of the body mistakenly attacks ...
... Semin Arthritis Rheum. 2010 Feb;39(4):257-68. ... Objectives: This review examines the burden and patterns of disease in systemic lupus erythematosus (SLE) and the influence and ... among nonwhite populations around the world and tends to be more severe in men and in pediatric and late-onset lupus. SLE ...
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Hospitalization of individuals with systemic lupus erythematosus: characteristics and predictors of outcome. Lupus 2003;12:672- ... The nature and outcome of infection in systemic lupus erythematosus. Lupus 2002;11:234-9. ... A structured literature review of the direct costs of adult systemic lupus erythematosus in the US. Arthritis Care Res 2011;63: ... Systemic lupus erythematosus (SLE) is a chronic auto-immune disease that predominantly affects women in their childbearing ...
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Background: Systemic Lupus Erythematosus (SLE) is a systemic autoimmune disease with diverse clinical manifestations. Although ... Transcription Factor Activity Inference in Systemic Lupus Erythematosus. life-11-00299-v2.pdf (1.766Mb). ... Transcription Factor Activity Inference in Systemic Lupus Erythematosus. Life 2021, 11, 299. https://doi.org/10.3390/ ...
Anti-dsDNA antibodies, S100A12, S100A8/A9, SLE glomerulonephritis, systemic lupus erythematosus. in Lupus. volume. 26. issue. 2 ... In Lupus 26(2). p.139-149 Abstract. Objectives Systemic lupus erythematosus (SLE) is associated with elevated levels of S100A8/ ... Objectives Systemic lupus erythematosus (SLE) is associated with elevated levels of S100A8/A9, pro-inflammatory proteins mainly ... Pro-inflammatory S100 proteins are associated with glomerulonephritis and anti-dsDNA antibodies in systemic lupus erythematosus ...
Systemic Lupus Erythematosus (SLE) - Etiology, pathophysiology, symptoms, signs, diagnosis & prognosis from the MSD Manuals - ... see Lupus Nephritis Lupus Nephritis Lupus nephritis is glomerulonephritis caused by systemic lupus erythematosus (SLE). ... Systemic Lupus Erythematosus (SLE) (Disseminated Lupus Erythematosus). By Alana M. Nevares , MD, The University of Vermont ... Variant Forms of Lupus Discoid lupus erythematosus (DLE) DLE, also sometimes called chronic cutaneous lupus erythematosus, is a ...
Severe lupus can cause harm to organs and other serious problems, including death. ... Systemic lupus erythematosus is a disease that causes your bodys immune system to attack its own cells and tissues. It can ... Understanding Systemic Lupus Erythematosus (Lupus) Systemic lupus erythematosus is an autoimmune disease that causes your ... Possible complications of lupus. Lupus can cause harm to the body over time. This can lead to serious problems, such as: * ...
2014). The Incidence and Prevalence of Systemic Lupus Erythematosus, 2002-2004: The Georgia Lupus Registry. 66(2). Lim, S. Sam ... "The Incidence and Prevalence of Systemic Lupus Erythematosus, 2002-2004: The Georgia Lupus Registry" 66, no. 2 (2014). Lim, S. ... The Incidence and Prevalence of Systemic Lupus Erythematosus, 2002-2004: The Georgia Lupus Registry Cite ... "The Incidence and Prevalence of Systemic Lupus Erythematosus, 2002-2004: The Georgia Lupus Registry" vol. 66, no. 2, 2014. ...
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5.7 Systemic Lupus Erythematosus. Thiazide diuretics have been reported to cause exacerbation or activation of systemic lupus ... A new or worsening condition called systemic lupus erythematosus (Lupus; SLE) * Eye problems. One of the medicines in HYZAAR ... 5.7 Systemic Lupus Erythematosus 6 ADVERSE REACTIONS 6.1 Clinical Trials Experience 6.2 Postmarketing Experience 7 DRUG ... The systemic bioavailability of losartan is approximately 33%. Mean peak concentrations of losartan and its active metabolite ...
Systemic lupus erythematosus (SLE) is a rheumatic disease characterized by autoantibodies directed against self-antigens, ... encoded search term (Pediatric Systemic Lupus Erythematosus) and Pediatric Systemic Lupus Erythematosus What to Read Next on ... validation of the Systemic Lupus International Collaborating Clinics classification criteria for systemic lupus erythematosus. ... Pediatric Systemic Lupus Erythematosus * Genetics of Systemic Lupus Erythematosus * Bullous Systemic Lupus Erythematosus (BSLE) ...
... Fagone, Paolo;Mangano, Katia;Di Marco ... Systemic lupus erythematosus (SLE) is a chronic inflammatory disease with various clinical features. Autoreactive B cells play ... Systemic lupus erythematosus (SLE) is a chronic inflammatory disease with various clinical features. Autoreactive B cells play ...
The objective of this work is to report and discuss the case of a patient who fulfilled the criteria for Systemic erythematosus ... Systemic erythematosus lupus (SLE) associated with a positive PR3-ANCA: A case report. 10th European Nephrology Conference. ... of this work is to report and discuss the case of a patient who fulfilled the criteria for Systemic erythematosus lupus (SLE) ... Lupus Nephritis Nephrosclerosis Paediatric Nephrology Renal Calculi Renal Carcinoma Renal Hypertension Renal Insufficiency ...
Anti-endothelial Cell Antibodies and Apoptosis in Systemic Lupus Erythematosus. *Savage, Caroline (Principal Investigator) ...
Systemic lupus erythematosus (SLE) is an autoimmune systemic disease and its pathogenesis has not yet been completely clarified ... Systemic lupus erythematosus (SLE) is an autoimmune systemic disease and its pathogenesis has not yet been completely clarified ... Role of the Specialized Proresolving Mediator Resolvin D1 in Systemic Lupus Erythematosus: Preliminary Results. Navarini L; ...
Systemic Lupus Erythematosus Pathogenesis: Interferon and Beyond Simone Caielli, Zurong Wan, and Virginia Pascual ...
BERNARDES, Vanessa Peter; OLIVEIRA, Lecila Duarte Barbosa y MARCON, Claudete. Juvenile systemic lupus erythematosus: diagnosis ... Palabras clave : Juvenile Systemic Lupus Erythematosus; Chronic Diseases; Family Relations; Hospitals. · resumen en Portugués ... to the recent statement of diagnosis and early treatment of a chronic disease called Juvenile Systemic Lupus Erythematosus. ...
Introduction: Systemic lupus erythematosus (SLE ) is a chronic inflammatory disease of unknown cause and autoimmune nature. The ... Study of characteristics and systemic stomatological in patients with lupus erythematosus. Rev. Assoc. Paul. Cir. Dent. [online ... Palavras-chave : oral health; lupus erythematosus; systemic pathological conditions; signs and symptoms; oral manifestations. ... The frequency, types of systemic damage, use of controlled medications used to treat this disease that undertake dental ...
... systemic lupus erythematosus). Systemic lupus erythematosus. Systemic lupus erythematosus (SLE) is an autoimmune disease. In ... Systemic diseases in which arthritis is a feature. In: Goldman L, Schafer AI, eds. Goldman-Cecil Medicine. 26th ed. ...
Systemic lupus erythematosus (SLE) is a chronic inflammatory autoimmune disorder associated with a wide range of symptoms and ... encoded search term (Genetics of Systemic Lupus Erythematosus) and Genetics of Systemic Lupus Erythematosus What to Read Next ... Genetics of systemic lupus erythematosus. Lupus. 1995 Dec. 4(6):425-37. [QxMD MEDLINE Link]. ... Complete complement deficiency in a large cohort of familial systemic lupus erythematosus. Lupus. 2010 Jan. 19(1):52-7. [QxMD ...
Uncommon lupus symptoms may include blood problems, strokes, and chest pain. Learn how to identify these symptoms and when to ... What is systemic lupus erythematosus (SLE)? (2021).. https://www.lupus.org/resources/what-is-systemic-lupus-erythematosus-sle. ... in 2018 investigated the prevalence of specific lupus symptoms among individuals living with systemic lupus erythematosus (SLE) ... According to the Lupus Foundation of America (LFA), lupus can cause a type of kidney disease called lupus nephritis (LN). ...
... and biopsy-proven lupus nephritis, leading to a second concomitant diagnosis of systemic lupus erythematosus (SLE). The ... and biopsy-proven lupus nephritis, leading to a second concomitant diagnosis of systemic lupus erythematosus (SLE). The ... and biopsy-proven lupus nephritis, leading to a second concomitant diagnosis of systemic lupus erythematosus (SLE). The ... and biopsy-proven lupus nephritis, leading to a second concomitant diagnosis of systemic lupus erythematosus (SLE). The ...
Uncoupling Protein 2 as genetic risk factor for systemic lupus erythematosus: association with malondialdehyde levels and ... Uncoupling Protein 2 as genetic risk factor for systemic lupus erythematosus: association with malondialdehyde levels and ... Uncoupling Protein 2 as genetic risk factor for systemic lupus erythematosus: association with malondialdehyde levels and ... the main cause of death in systemic lupus erythematous (SLE). To gain insight into these mechanisms, we studied the association ...
... is a common systemic autoimmune disease with a complex genetic inheritance. Genome-wide association studies (GWAS) have ... Systemic lupus erythematosus (SLE) is a common systemic autoimmune disease with a complex genetic inheritance. Genome-wide ... Systemic lupus erythematosus (SLE [MIM: 152700]) is a common systemic autoimmune disease characterized by the production of ... Danchenko N, Satia J, Anthony M. Epidemiology of systemic lupus erythematosus: a comparison of worldwide disease burden. Lupus ...
  • Netting neutrophils are major inducers of type I IFN production in pediatric systemic lupus erythematosus. (medscape.com)
  • A proposed framework to standardize the neurocognitive assessment of patients with pediatric systemic lupus erythematosus. (medscape.com)
  • The prevalence of scleroderma was 0.2% (RR 15.65, 95% CL 0.21-87.03) and the prevalence of systemic lupus erythematosus was 0.2% (RR 11.37, 95% CL 0.15-63.23). (cdc.gov)
  • Rheumatoid Arthritis (RA) Rheumatoid arthritis is a chronic systemic autoimmune disease that primarily involves the joints. (msdmanuals.com)
  • A 2016 meta-analysis found that Sjogren's syndrome is associated with an increased risk of developing certain types of autoimmune diseases, including systemic lupus erythematosus, rheumatoid arthritis and antiphospholipid syndrome. (disabilityworks.org)
  • It has also been speculated that Sjogren's Syndrome may increase a person's risk for developing certain auto-immune diseases such as rheumatoid arthritis, lupus and thyroid disease though-out their life span. (disabilityworks.org)
  • There were 24 people with rheumatoid arthritis, one with scleroderma, and one with systemic lupus erythematosus. (cdc.gov)
  • Conclusion: Although the association between scleroderma and silicosis has been more widely reported in the literature, the prevalence of rheumatoid arthritis was greater than the prevalence of scleroderma or systemic lupus erythematosus among a cohort of individuals with silicosis. (cdc.gov)
  • tell your doctor if you have or have ever had an autoimmune disorder (conditions in which the immune system attacks healthy parts of the body and causes pain, swelling, and damage) such as rheumatoid arthritis, systemic lupus erythematosus, or nephritis (a type of kidney problem). (safemedication.com)
  • Between July 2021 and September 2021, 265 patients were enrolled, including patients with Sjogren's syndrome (n=49), rheumatoid arthritis (n=34), systemic lupus erythematosus (n=33), spondyloarthritis (n=21) and other rheumatic diseases (online supplemental table S1). (bmj.com)
  • Have you heard of osteoarthritis, rheumatoid arthritis, ankylosing spondylitis, psoriatic arthritis, systemic lupus erythematosus, gout, and childhood or juvenile idiopathic arthritis-all types of arthritis disease? (arthritisresearch.ca)
  • The role of extracellular RNA in the pathogenesis and therapy in systemic lupus erythematosus has been extensively addressed. (biomedcentral.com)
  • This study reviewed the importance of less explored lesions by the current and widely used 2003 classification of lupus nephritis of the International Society of Nephrology /Renal Pathology Society (ISN/RPS), with emphasis on the tubulointerstitial, podocyte , and vascular lesions, increasingly recognised as being important in the pathogenesis and prognosis of the disease . (bvsalud.org)
  • The American and European Rheumatology societies have published classification criteria to assist the diagnosis of lupus. (medlineplus.gov)
  • Updating the American College of Rheumatology revised criteria for the classification of systemic lupus erythematosus. (medscape.com)
  • Because of its protean manifestations, lupus must be considered in the differential diagnoses of many conditions, including fevers of unknown origin, arthralgia, anemia , new-onset kidney disease, psychosis, and fatigue. (medscape.com)
  • He also addresses the significance of the Toll-like receptors, and how they complicate intracellular trash collection inside individuals who are genetically susceptible to lupus and other autoimmune diseases. (hcplive.com)
  • Diagnostic laboratory studies include antinuclear antibody (ANA), anti-double-stranded DNA, anti-Smith antibody, lupus anticoagulant, and antiphospholipid antibody panel. (medscape.com)
  • Predictive value of persistent versus transient antiphospholipid antibody subtypes for the risk of thrombotic events in pediatric patients with systemic lupus erythematosus. (medscape.com)
  • Management of neuropsychiatric lupus is similar to the management of neuropsychiatric disease in patients without lupus. (wikipedia.org)
  • Systemic lupus erythematosus (SLE) is an autoimmune disease . (medlineplus.gov)
  • Development and assessment of a computerized index of clinical disease activity in systemic lupus erythematosus. (nih.gov)
  • Five centres in Great Britain and the Republic of Ireland have collaborated to produce a computerized index of clinical disease activity in systemic lupus erythematosus, based on the principle of the physician's intention to treat. (nih.gov)
  • It has great potential for use in multicentre studies of disease outcome and new therapies in systemic lupus erythematosus. (nih.gov)
  • Systemic lupus erythematosus (SLE) is a rheumatic disease characterized by autoantibodies directed against self-antigens, immune complex formation, and immune dysregulation, resulting in damage to essentially any organ. (medscape.com)
  • Osler was the first physician who recognized that systemic features of the disease could occur without skin involvement. (medscape.com)
  • Worsening disease activity was predicted by rises in serum BLyS concentrations using the Safety of Estrogen in Lupus Erythematosus National Assessment-SLE Disease Activity Index (SELENA-SLEDAI) and elevated anti-dsDNA antibody titers 15 . (jrheum.org)
  • Background: Systemic Lupus Erythematosus (SLE) is a systemic autoimmune disease with diverse clinical manifestations. (ugr.es)
  • Indeed, in some cases, HLA genes are more highly related to lupus-associated autoantibodies than to the disease itself. (medscape.com)
  • Systemic lupus erythematosus (SLE) is a kind of autoimmune disease that has protean manifestations. (biomedcentral.com)
  • Nguyen, MA, Rahnama-Moghadam, S & Gilson, RT 2016, ' An uncommon presentation of an uncommon disease: Relapsing polychondritis overlap with systemic lupus erythematosus ', Dermatology online journal , vol. 22, no. 2. (uthscsa.edu)
  • Systemic lupus erythematosus (SLE) is a common systemic autoimmune disease with a complex genetic inheritance. (biomedcentral.com)
  • Systemic lupus erythematosus (SLE [MIM: 152700]) is a common systemic autoimmune disease characterized by the production of autoantibodies and a complex genetic inheritance. (biomedcentral.com)
  • This article presents the report of psychological intervention in the pediatric ward of a school hospital, referring to the recent statement of diagnosis and early treatment of a chronic disease called Juvenile Systemic Lupus Erythematosus. (bvsalud.org)
  • Introduction: Systemic lupus erythematosus (SLE ) is a chronic inflammatory disease of unknown cause and autoimmune nature. (bvsalud.org)
  • The frequency, types of systemic damage, use of controlled medications used to treat this disease that undertake dental treatment. (bvsalud.org)
  • Transmission an incidence rate of 1.5 cases/1,000 live births and a of T. gondii can occur through food items and the en- burden of disease of 1.2 million disease-adjusted life vironment. (cdc.gov)
  • Hydralazine has been in use as a treatment for hypertension, most notably in heart failure patients, since 1951.1 The drug is a known cause of autoimmune disease, most specifically hydralazine-induced lupus. (the-rheumatologist.org)
  • These syndromes encompass disorders of the central and peripheral nervous systems: Each of the 19 syndromes are also stand-alone diagnoses, which can occur with or without lupus. (wikipedia.org)
  • Conclusion: The oral health of the patients is poor, there is great variability in systemic diseases, use of various drugs with negative side effects and immunosuppressants for the general condition of patients with SLE. (bvsalud.org)
  • The main diagnostic categories for FUO include infections (local, systemic), neoplasms, and collagen-vascular (immune-mediated) diseases. (vin.com)
  • Systemic mycotic diseases (e.g., histoplasmosis, blastomycosis, coccidioidomycosis) cause antibiotic unresponsive fever and should be included in the differential list for patients residing in or having traveled through regions endemic for these agents. (vin.com)
  • We came to the insight that DNA and RNA, which are the essential major targets in lupus and actually in several auto-immune diseases, carry with themselves the kind of danger signals that are also present in viruses and bacteria. (hcplive.com)
  • We and many others have felt that it comes from dead and dying cells that may not be so efficiently cleared in diseases like lupus. (hcplive.com)
  • Further investigations revealed positive ANA and anti-Smith antibody, oral ulcers, a photo-distributed skin eruption, and biopsy-proven lupus nephritis, leading to a second concomitant diagnosis of systemic lupus erythematosus (SLE). (uthscsa.edu)
  • Identification of a urinary proteomic signature for lupus nephritis in children. (medscape.com)
  • A common criticism of the classification of lupus nephritis is the relative scarcity of information regarding tubular, interstitial, and vascular changes compared to the available information regarding glomerular changes, even though their potential for independent progression is known. (bvsalud.org)
  • Systemic lupus erythematosus is a chronic, multisystem, inflammatory disorder of autoimmune etiology, occurring predominantly in young women. (msdmanuals.com)
  • In addition, onset of neuropsychiatric symptoms may happen prior to the diagnosis of lupus. (wikipedia.org)
  • There are several possible mechanisms that underlie the nervous system manifestations of lupus. (wikipedia.org)
  • The use of the New Zealand black/white mouse model, which manifested spontaneous Coombs-positive anemia and many other manifestations of lupus, has allowed intensive study of SLE's mechanisms and the importance of immunosuppressive therapy. (medscape.com)
  • To evaluate the efficacy/safety of belimumab plus standard therapy in patients (n = 449) with active systemic lupus erythematosus (SLE) treated up to 7 years (n = 177 currently ongoing). (jrheum.org)
  • Systemic lupus erythematosus (SLE) is a chronic auto-immune disorder characterized by autoantibody production and abnormal B lymphocyte function 1 . (jrheum.org)
  • Systemic Lupus Erythematosus (SLE) is a chronic inflammatory autoimmune disorder associated with a wide range of symptoms and physical findings. (medscape.com)
  • Derivation and validation of the Systemic Lupus International Collaborating Clinics classification criteria for systemic lupus erythematosus. (medscape.com)
  • Systemic lupus erythematosus (SLE) is more common and severe among Black and Asian patients than among White patients. (msdmanuals.com)
  • Vallin H, Blomberg S, Alm GV, Cederblad B, Rönnblom L. Patients with systemic lupus erythematosus (SLE) have a circulating inducer of interferon-alpha (IFN-alpha) production acting on leucocytes resembling immature dendritic cells. (medscape.com)
  • The use of multiple medications and the presence of multiple systemic changes may compromise the dental care of these patients especially when they are uncompensated and debilitated. (bvsalud.org)
  • Methods: 34 patients were analyzed with SLE that were submitted a structured interview about systemic condition and dental exam: DMFT index, gingival health condition and temporo mandibular joint pain. (bvsalud.org)
  • Recognition of these lesions can help with therapeutic decision -making, thereby allowing better results for patients with systemic lupus erythematosus . (bvsalud.org)
  • Though neuropsychiatric lupus is sometimes referred to as "CNS lupus", it can also affect the peripheral nervous system (PNS). (wikipedia.org)
  • These medicines are used if you have severe lupus that is affecting the nervous system, kidney, or other organs. (medlineplus.gov)
  • Hydralazine-induced lupus occurs in 7-13% of those taking the medication.2-4 It often presents with constitutional symptoms, arthritis/arthralgias, cutaneous lesions, sero-sitis, myalgias and/or hepatomegaly. (the-rheumatologist.org)
  • Some drugs (eg, hydralazine , procainamide , isoniazid , anti-tumor necrosis factor [TNF] drugs) cause a reversible lupus-like syndrome. (msdmanuals.com)
  • AUDIO) Dr. Mark Shlomchik has won the first $200,000 Insight Prize for research that led toward new lupus drugs such as belimumab. (hcplive.com)
  • Objectives Systemic lupus erythematosus (SLE) is associated with elevated levels of S100A8/A9, pro-inflammatory proteins mainly secreted by activated polymorphonuclear neutrophils (PMNs). (lu.se)
  • Skin involvement is most frequently linked to concomitant myelodysplastic syndrome and has rarely been associated with systemic lupus erythematosus. (uthscsa.edu)
  • Renal involvement in systemic lupus erythematosus: additional histopathological lesions. (bvsalud.org)
  • What causes the immune system to misfire so disastrously in disorders like lupus? (hcplive.com)
  • Systemic lupus erythematosus (SLE), is the most common type of lupus. (cdc.gov)
  • It is helpful to categorize infections as either localized or systemic in order to allow for an eventual well-focused approach to the patient's problem. (vin.com)
  • If all goes well, their work may lead a new understanding of the puzzling association between lupus flares and infections. (hcplive.com)
  • In a brief recorded interview, hear how the award may help him find an explanation for the links between infection and lupus. (hcplive.com)
  • For insights that helped lead the way to solutions named rituximab and belimumab, Mark Shlomchik MD PhD has been named the first recipient of the new $200,000 Insight Prize awarded by a trio of related institutions: the Alliance for Lupus Research, the Lupus Foundation of America , and the Lupus Research Institute . (hcplive.com)
  • Learn more about lupus diagnosis and treatment . (cdc.gov)