Antibodies that react with self-antigens (AUTOANTIGENS) of the organism that produced them.
Endogenous tissue constituents that have the ability to interact with AUTOANTIBODIES and cause an immune response.
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.
Disorders that are characterized by the production of antibodies that react with host tissues or immune effector cells that are autoreactive to endogenous peptides.
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.
The major immunoglobulin isotype class in normal human serum. There are several isotype subclasses of IgG, for example, IgG1, IgG2A, and IgG2B.
Process whereby the immune system reacts against the body's own tissues. Autoimmunity may produce or be caused by AUTOIMMUNE DISEASES.
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.
Group of chronic blistering diseases characterized histologically by ACANTHOLYSIS and blister formation within the EPIDERMIS.
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.
Antibodies specific to INSULIN.
A pyridoxal-phosphate protein that catalyzes the alpha-decarboxylation of L-glutamic acid to form gamma-aminobutyric acid and carbon dioxide. The enzyme is found in bacteria and in invertebrate and vertebrate nervous systems. It is the rate-limiting enzyme in determining GAMMA-AMINOBUTYRIC ACID levels in normal nervous tissues. The brain enzyme also acts on L-cysteate, L-cysteine sulfinate, and L-aspartate. EC 4.1.1.15.
A chronic and relatively benign subepidermal blistering disease usually of the elderly and without histopathologic acantholysis.
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 desmosomal cadherin that is an autoantigen in the acquired skin disorder PEMPHIGUS VULGARIS.
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.
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.
Sites on an antigen that interact with specific antibodies.
Antibodies found in adult RHEUMATOID ARTHRITIS patients that are directed against GAMMA-CHAIN IMMUNOGLOBULINS.
A form of cutaneous tuberculosis. It is seen predominantly in women and typically involves the NASAL MUCOSA; BUCCAL MUCOSA; and conjunctival mucosa.
Acquired hemolytic anemia due to the presence of AUTOANTIBODIES which agglutinate or lyse the patient's own RED BLOOD CELLS.
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).
Small RNAs found in the cytoplasm usually complexed with proteins in scRNPs (RIBONUCLEOPROTEINS, SMALL CYTOPLASMIC).
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.
Inflammation of a muscle or muscle tissue.
A family of structurally-related short-chain collagens that do not form large fibril bundles.
A subclass of receptor-like protein tryosine phosphatases that contain an extracellular RDGS-adhesion recognition motif and a single cytosolic protein tyrosine phosphate domain.
A subtype of DIABETES MELLITUS that is characterized by INSULIN deficiency. It is manifested by the sudden onset of severe HYPERGLYCEMIA, rapid progression to DIABETIC KETOACIDOSIS, and DEATH unless treated with insulin. The disease may occur at any age, but is most common in childhood or adolescence.
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 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.
Inflammatory disease of the THYROID GLAND due to autoimmune responses leading to lymphocytic infiltration of the gland. It is characterized by the presence of circulating thyroid antigen-specific T-CELLS and thyroid AUTOANTIBODIES. The clinical signs can range from HYPOTHYROIDISM to THYROTOXICOSIS depending on the type of autoimmune thyroiditis.
A desmosomal cadherin that is an autoantigen in the acquired skin disorder PEMPHIGUS FOLIACEUS.
Complexes of RNA-binding proteins with ribonucleic acids (RNA).
A subacute or chronic inflammatory disease of muscle and skin, marked by proximal muscle weakness and a characteristic skin rash. The illness occurs with approximately equal frequency in children and adults. The skin lesions usually take the form of a purplish rash (or less often an exfoliative dermatitis) involving the nose, cheeks, forehead, upper trunk, and arms. The disease is associated with a complement mediated intramuscular microangiopathy, leading to loss of capillaries, muscle ischemia, muscle-fiber necrosis, and perifascicular atrophy. The childhood form of this disease tends to evolve into a systemic vasculitis. Dermatomyositis may occur in association with malignant neoplasms. (From Adams et al., Principles of Neurology, 6th ed, pp1405-6)
Autoantibodies directed against cytoplasmic constituents of POLYMORPHONUCLEAR LEUKOCYTES and/or MONOCYTES. They are used as specific markers for GRANULOMATOSIS WITH POLYANGIITIS and other diseases, though their pathophysiological role is not clear. ANCA are routinely detected by indirect immunofluorescence with three different patterns: c-ANCA (cytoplasmic), p-ANCA (perinuclear), and atypical ANCA.
Methods used for studying the interactions of antibodies with specific regions of protein antigens. Important applications of epitope mapping are found within the area of immunochemistry.
In patients with neoplastic diseases a wide variety of clinical pictures which are indirect and usually remote effects produced by tumor cell metabolites or other products.
A test to detect non-agglutinating ANTIBODIES against ERYTHROCYTES by use of anti-antibodies (the Coombs' reagent.) The direct test is applied to freshly drawn blood to detect antibody bound to circulating red cells. The indirect test is applied to serum to detect the presence of antibodies that can bind to red blood cells.
A hemeprotein that catalyzes the oxidation of the iodide radical to iodine with the subsequent iodination of many organic compounds, particularly proteins. EC 1.11.1.8.
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.
Local surface sites on antibodies which react with antigen determinant sites on antigens (EPITOPES.) They are formed from parts of the variable regions of FAB FRAGMENTS.
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.
The processes triggered by interactions of ANTIBODIES with their ANTIGENS.
Antibodies produced by a single clone of cells.
Serological reactions in which an antiserum against one antigen reacts with a non-identical but closely related antigen.
A common form of hyperthyroidism with a diffuse hyperplastic GOITER. It is an autoimmune disorder that produces antibodies against the THYROID STIMULATING HORMONE RECEPTOR. These autoantibodies activate the TSH receptor, thereby stimulating the THYROID GLAND and hypersecretion of THYROID HORMONES. These autoantibodies can also affect the eyes (GRAVES OPHTHALMOPATHY) and the skin (Graves dermopathy).
Antibodies which react with the individual structural determinants (idiotopes) on the variable region of other antibodies.
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.
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).
Autoimmune diseases affecting multiple endocrine organs. Type I is characterized by childhood onset and chronic mucocutaneous candidiasis (CANDIDIASIS, CHRONIC MUCOCUTANEOUS), while type II exhibits any combination of adrenal insufficiency (ADDISON'S DISEASE), lymphocytic thyroiditis (THYROIDITIS, AUTOIMMUNE;), HYPOPARATHYROIDISM; and gonadal failure. In both types organ-specific ANTIBODIES against a variety of ENDOCRINE GLANDS have been detected. The type II syndrome differs from type I in that it is associated with HLA-A1 and B8 haplotypes, onset is usually in adulthood, and candidiasis is not present.
A form of fluorescent antibody technique commonly used to detect serum antibodies and immune complexes in tissues and microorganisms in specimens from patients with infectious diseases. The technique involves formation of an antigen-antibody complex which is labeled with fluorescein-conjugated anti-immunoglobulin antibody. (From Bennington, Saunders Dictionary & Encyclopedia of Laboratory Medicine and Technology, 1984)
Skin diseases characterized by local or general distributions of blisters. They are classified according to the site and mode of blister formation. Lesions can appear spontaneously or be precipitated by infection, trauma, or sunlight. Etiologies include immunologic and genetic factors. (From Scientific American Medicine, 1990)
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.
A condition characterized by persistent spasms (SPASM) involving multiple muscles, primarily in the lower limbs and trunk. The illness tends to occur in the fourth to sixth decade of life, presenting with intermittent spasms that become continuous. Minor sensory stimuli, such as noise and light touch, precipitate severe spasms. Spasms do not occur during sleep and only rarely involve cranial muscles. Respiration may become impaired in advanced cases. (Adams et al., Principles of Neurology, 6th ed, p1492; Neurology 1998 Jul;51(1):85-93)
Diseases characterized by inflammation involving multiple muscles. This may occur as an acute or chronic condition associated with medication toxicity (DRUG TOXICITY); CONNECTIVE TISSUE DISEASES; infections; malignant NEOPLASMS; and other disorders. The term polymyositis is frequently used to refer to a specific clinical entity characterized by subacute or slowly progressing symmetrical weakness primarily affecting the proximal limb and trunk muscles. The illness may occur at any age, but is most frequent in the fourth to sixth decade of life. Weakness of pharyngeal and laryngeal muscles, interstitial lung disease, and inflammation of the myocardium may also occur. Muscle biopsy reveals widespread destruction of segments of muscle fibers and an inflammatory cellular response. (Adams et al., Principles of Neurology, 6th ed, pp1404-9)
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.
Inflammation of any one of the blood vessels, including the ARTERIES; VEINS; and rest of the vasculature system in the body.
A highly vascularized endocrine gland consisting of two lobes joined by a thin band of tissue with one lobe on each side of the TRACHEA. It secretes THYROID HORMONES from the follicular cells and CALCITONIN from the parafollicular cells thereby regulating METABOLISM and CALCIUM level in blood, respectively.
FIBROSIS of the hepatic parenchyma due to obstruction of BILE flow (CHOLESTASIS) in the intrahepatic or extrahepatic bile ducts (BILE DUCTS, INTRAHEPATIC; BILE DUCTS, EXTRAHEPATIC). Primary biliary cirrhosis involves the destruction of small intra-hepatic bile ducts and bile secretion. Secondary biliary cirrhosis is produced by prolonged obstruction of large intrahepatic or extrahepatic bile ducts from a variety of causes.
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 polymorphonuclear leukocyte-derived serine protease that degrades proteins such as ELASTIN; FIBRONECTIN; LAMININ; VITRONECTIN; and COLLAGEN. It is named for its ability to control myeloid cell growth and differentiation.
Cell surface proteins that bind pituitary THYROTROPIN (also named thyroid stimulating hormone or TSH) and trigger intracellular changes of the target cells. TSH receptors are present in the nervous system and on target cells in the thyroid gland. Autoantibodies to TSH receptors are implicated in thyroid diseases such as GRAVES DISEASE and Hashimoto disease (THYROIDITIS, AUTOIMMUNE).
Ligand-binding assays that measure protein-protein, protein-small molecule, or protein-nucleic acid interactions using a very large set of capturing molecules, i.e., those attached separately on a solid support, to measure the presence or interaction of target molecules in the sample.
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.
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.
Descriptions of specific amino acid, carbohydrate, or nucleotide sequences which have appeared in the published literature and/or are deposited in and maintained by databanks such as GENBANK, European Molecular Biology Laboratory (EMBL), National Biomedical Research Foundation (NBRF), or other sequence repositories.
A chronic self-perpetuating hepatocellular INFLAMMATION of unknown cause, usually with HYPERGAMMAGLOBULINEMIA and serum AUTOANTIBODIES.
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.
Visible accumulations of fluid within or beneath the epidermis.
The production of ANTIBODIES by proliferating and differentiated B-LYMPHOCYTES under stimulation by ANTIGENS.
Represents 15-20% of the human serum immunoglobulins, mostly as the 4-chain polymer in humans or dimer in other mammals. Secretory IgA (IMMUNOGLOBULIN A, SECRETORY) is the main immunoglobulin in secretions.
Form of epidermolysis bullosa characterized by trauma-induced, subepidermal blistering with no family history of the disease. Direct immunofluorescence shows IMMUNOGLOBULIN G deposited at the dermo-epidermal junction.
The order of amino acids as they occur in a polypeptide chain. This is referred to as the primary structure of proteins. It is of fundamental importance in determining PROTEIN CONFORMATION.
Immunologic method used for detecting or quantifying immunoreactive substances. The substance is identified by first immobilizing it by blotting onto a membrane and then tagging it with labeled antibodies.
An enzyme that activates histidine with its specific transfer RNA. EC 6.1.1.21.
Pathological processes involving the THYROID GLAND.
Inflammatory diseases of the THYROID GLAND. Thyroiditis can be classified into acute (THYROIDITIS, SUPPURATIVE), subacute (granulomatous and lymphocytic), chronic fibrous (Riedel's), chronic lymphocytic (HASHIMOTO DISEASE), transient (POSTPARTUM THYROIDITIS), and other AUTOIMMUNE THYROIDITIS subtypes.
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.
Mercury chloride (HgCl2). A highly toxic compound that volatizes slightly at ordinary temperature and appreciably at 100 degrees C. It is corrosive to mucous membranes and used as a topical antiseptic and disinfectant.
An autoimmune disease of the KIDNEY and the LUNG. It is characterized by the presence of circulating autoantibodies targeting the epitopes in the non-collagenous domains of COLLAGEN TYPE IV in the basement membranes of kidney glomeruli (KIDNEY GLOMERULUS) and lung alveoli (PULMONARY ALVEOLI), and the subsequent destruction of these basement membranes. Clinical features include pulmonary alveolar hemorrhage and glomerulonephritis.
Univalent antigen-binding fragments composed of one entire IMMUNOGLOBULIN LIGHT CHAIN and the amino terminal end of one of the IMMUNOGLOBULIN HEAVY CHAINS from the hinge region, linked to each other by disulfide bonds. Fab contains the IMMUNOGLOBULIN VARIABLE REGIONS, which are part of the antigen-binding site, and the first IMMUNOGLOBULIN CONSTANT REGIONS. This fragment can be obtained by digestion of immunoglobulins with the proteolytic enzyme PAPAIN.
Transmembrane proteins that form the beta subunits of the HLA-DQ antigens.
A group of the D-related HLA antigens found to differ from the DR antigens in genetic locus and therefore inheritance. These antigens are polymorphic glycoproteins comprising alpha and beta chains and are found on lymphoid and other cells, often associated with certain diseases.
An adrenal disease characterized by the progressive destruction of the ADRENAL CORTEX, resulting in insufficient production of ALDOSTERONE and HYDROCORTISONE. Clinical symptoms include ANOREXIA; NAUSEA; WEIGHT LOSS; MUSCLE WEAKNESS; and HYPERPIGMENTATION of the SKIN due to increase in circulating levels of ACTH precursor hormone which stimulates MELANOCYTES.
Disorders of connective tissue, especially the joints and related structures, characterized by inflammation, degeneration, or metabolic derangement.
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.
A PULMONARY ALVEOLI-filling disease, characterized by dense phospholipoproteinaceous deposits in the alveoli, cough, and DYSPNEA. This disease is often related to, congenital or acquired, impaired processing of PULMONARY SURFACTANTS by alveolar macrophages, a process dependent on GRANULOCYTE-MACROPHAGE COLONY-STIMULATING FACTOR.
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.
That region of the immunoglobulin molecule that varies in its amino acid sequence and composition, and comprises the binding site for a specific antigen. It is located at the N-terminus of the Fab fragment of the immunoglobulin. It includes hypervariable regions (COMPLEMENTARITY DETERMINING REGIONS) and framework regions.
Genetically identical individuals developed from brother and sister matings which have been carried out for twenty or more generations, or by parent x offspring matings carried out with certain restrictions. All animals within an inbred strain trace back to a common ancestor in the twentieth generation.
A disorder of neuromuscular transmission characterized by weakness of cranial and skeletal muscles. Autoantibodies directed against acetylcholine receptors damage the motor endplate portion of the NEUROMUSCULAR JUNCTION, impairing the transmission of impulses to skeletal muscles. Clinical manifestations may include diplopia, ptosis, and weakness of facial, bulbar, respiratory, and proximal limb muscles. The disease may remain limited to the ocular muscles. THYMOMA is commonly associated with this condition. (Adams et al., Principles of Neurology, 6th ed, p1459)
A technique using antibodies for identifying or quantifying a substance. Usually the substance being studied serves as antigen both in antibody production and in measurement of antibody by the test substance.
The classes of immunoglobulins found in any species of animal. In man there are nine classes that migrate in five different groups in electrophoresis; they each consist of two light and two heavy protein chains, and each group has distinguishing structural and functional properties.
Abnormal immunoglobulins, especially IGG or IGM, that precipitate spontaneously when SERUM is cooled below 37 degrees Celsius. It is characteristic of CRYOGLOBULINEMIA.
Separation of the prickle cells of the stratum spinosum of the epidermis, resulting in atrophy of the prickle cell layer. It is seen in diseases such as pemphigus vulgaris (see PEMPHIGUS) and DARIER DISEASE.
The structure of one molecule that imitates or simulates the structure of a different molecule.
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).
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.
A measure of the binding strength between antibody and a simple hapten or antigen determinant. It depends on the closeness of stereochemical fit between antibody combining sites and antigen determinants, on the size of the area of contact between them, and on the distribution of charged and hydrophobic groups. It includes the concept of "avidity," which refers to the strength of the antigen-antibody bond after formation of reversible complexes.
A syndrome characterized by acute OPTIC NEURITIS; MYELITIS, TRANSVERSE; demyelinating and/or necrotizing lesions in the OPTIC NERVES and SPINAL CORD; and presence of specific autoantibodies to AQUAPORIN 4.
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).
Irregular microscopic structures consisting of cords of endocrine cells that are scattered throughout the PANCREAS among the exocrine acini. Each islet is surrounded by connective tissue fibers and penetrated by a network of capillaries. There are four major cell types. The most abundant beta cells (50-80%) secrete INSULIN. Alpha cells (5-20%) secrete GLUCAGON. PP cells (10-35%) secrete PANCREATIC POLYPEPTIDE. Delta cells (~5%) secrete SOMATOSTATIN.
Thrombocytopenia occurring in the absence of toxic exposure or a disease associated with decreased platelets. It is mediated by immune mechanisms, in most cases IMMUNOGLOBULIN G autoantibodies which attach to platelets and subsequently undergo destruction by macrophages. The disease is seen in acute (affecting children) and chronic (adult) forms.
A multisystemic disease of a complex genetic background. It is characterized by inflammation of the blood vessels (VASCULITIS) leading to damage in any number of organs. The common features include granulomatous inflammation of the RESPIRATORY TRACT and kidneys. Most patients have measurable autoantibodies (ANTINEUTROPHIL CYTOPLASMIC ANTIBODIES) against neutrophil proteinase-3 (WEGENER AUTOANTIGEN).
Cells artificially created by fusion of activated lymphocytes with neoplastic cells. The resulting hybrid cells are cloned and produce pure MONOCLONAL ANTIBODIES or T-cell products, identical to those produced by the immunologically competent parent cell.
Aquaporin 4 is the major water-selective channel in the CENTRAL NERVOUS SYSTEM of mammals.
Autoantibodies that bind to the thyroid-stimulating hormone (TSH) receptor (RECEPTORS, THYROTROPIN) on thyroid epithelial cells. The autoantibodies mimic TSH causing an unregulated production of thyroid hormones characteristic of GRAVES DISEASE.
Identification of proteins or peptides that have been electrophoretically separated by blot transferring from the electrophoresis gel to strips of nitrocellulose paper, followed by labeling with antibody probes.
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.
Transglutaminases catalyze cross-linking of proteins at a GLUTAMINE in one chain with LYSINE in another chain. They include keratinocyte transglutaminase (TGM1 or TGK), tissue transglutaminase (TGM2 or TGC), plasma transglutaminase involved with coagulation (FACTOR XIII and FACTOR XIIIa), hair follicle transglutaminase, and prostate transglutaminase. Although structures differ, they share an active site (YGQCW) and strict CALCIUM dependence.
Substances that are recognized by the immune system and induce an immune reaction.
Antigenic determinants recognized and bound by the B-cell receptor. Epitopes recognized by the B-cell receptor are located on the surface of the antigen.
Peptides whose amino and carboxy ends are linked together with a peptide bond forming a circular chain. Some of them are ANTI-INFECTIVE AGENTS. Some of them are biosynthesized non-ribosomally (PEPTIDE BIOSYNTHESIS, NON-RIBOSOMAL).
A subclass of beta-adrenergic receptors (RECEPTORS, ADRENERGIC, BETA). The adrenergic beta-1 receptors are equally sensitive to EPINEPHRINE and NOREPINEPHRINE and bind the agonist DOBUTAMINE and the antagonist METOPROLOL with high affinity. They are found in the HEART, juxtaglomerular cells, and in the central and peripheral nervous systems.
Cell surface receptors that bind to and internalize SECRETED PHOSPHOLIPASES A2. Although primarily acting as scavenger receptors, these proteins may also play a role in intracellular signaling. Soluble forms of phospholipase A2 receptors occur through the action of proteases and may a play a role in the inhibition of extracellular phospholipase activity.
Proteins prepared by recombinant DNA technology.
An encapsulated lymphatic organ through which venous blood filters.
A classification of B-lymphocytes based on structurally or functionally different populations of cells.
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.
The normal lack of the ability to produce an immunological response to autologous (self) antigens. A breakdown of self tolerance leads to autoimmune diseases. The ability to recognize the difference between self and non-self is the prime function of the immune system.
Sensitive assay using radiolabeled ANTIGENS to detect specific ANTIBODIES in SERUM. The antigens are allowed to react with the serum and then precipitated using a special reagent such as PROTEIN A sepharose beads. The bound radiolabeled immunoprecipitate is then commonly analyzed by gel electrophoresis.
Immunologically detectable substances found in the CELL NUCLEUS.
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.
An HLA-DR antigen which is associated with HLA-DRB1 CHAINS encoded by DRB1*03 alleles.
A malabsorption syndrome that is precipitated by the ingestion of foods containing GLUTEN, such as wheat, rye, and barley. It is characterized by INFLAMMATION of the SMALL INTESTINE, loss of MICROVILLI structure, failed INTESTINAL ABSORPTION, and MALNUTRITION.
The largest of polypeptide chains comprising immunoglobulins. They contain 450 to 600 amino acid residues per chain, and have molecular weights of 51-72 kDa.

Weak autoantibody reactions to antigens other than sperm after vasectomy. (1/9574)

Autoantibody activity against various antigens was measured by indirect immunofluorescence in 97 men about to undergo vasectomy and 170 men who had undergone the operation up to six years earlier. There was a significantly higher prevalence of weakly positive autoantibody reactions among those who had undergone vasectomy. There was, however, no evidence that vasectomy could induce stronger autoantibody reactions such as those associated with autoimmune disease.  (+info)

Anti-heart autoantibodies in ischaemic heart disease patients. (2/9574)

One hundred and ninety-nine ischaemic heart disease (IHD) patients were studied with regard to the prevalence of anti-heart autoantibodies (AHA). The incidence of AHA in IHD patients was 1%: one out of 102 patients who suffered acute myocardial infarction (AMI), one out of seventy-two patients who suffered from acute coronary insufficiency (ACI), and none out of twenty-five patients with other signs and symptoms of IHD, had AHA in their sera. An additional 2% of patients who suffered from AMI developed detectable antibody levels during a follow-up period of 15 days. In comparison,, 53% of patients (eight out of fifteen) who underwent heart surgery and who had no AHA prior to operation, developed these antibodies in their sera during 1-2 weeks following operation.  (+info)

Explanations for the clinical and microscopic localization of lesions in pemphigus foliaceus and vulgaris. (3/9574)

Patients with pemphigus foliaceus (PF) have blisters on skin, but not mucous membranes, whereas patients with pemphigus vulgaris (PV) develop blisters on mucous membranes and/or skin. PF and PV blisters are due to loss of keratinocyte cell-cell adhesion in the superficial and deep epidermis, respectively. PF autoantibodies are directed against desmoglein (Dsg) 1; PV autoantibodies bind Dsg3 or both Dsg3 and Dsg1. In this study, we test the hypothesis that coexpression of Dsg1 and Dsg3 in keratinocytes protects against pathology due to antibody-induced dysfunction of either one alone. Using passive transfer of pemphigus IgG to normal and DSG3(null) neonatal mice, we show that in the areas of epidermis and mucous membrane that coexpress Dsg1 and Dsg3, antibodies against either desmoglein alone do not cause spontaneous blisters, but antibodies against both do. In areas (such as superficial epidermis of normal mice) where Dsg1 without Dsg3 is expressed, anti-Dsg1 antibodies alone can cause blisters. Thus, the anti-desmoglein antibody profiles in pemphigus sera and the normal tissue distributions of Dsg1 and Dsg3 determine the sites of blister formation. These studies suggest that pemphigus autoantibodies inhibit the adhesive function of desmoglein proteins, and demonstrate that either Dsg1 or Dsg3 alone is sufficient to maintain keratinocyte adhesion.  (+info)

Autoantibodies to gastrin in patients with pernicious anaemia--a novel antibody. (4/9574)

Autoantibodies arise when there is a breakdown in immunological tolerance. Autoantibodies to parietal cells and intrinsic factor are found in autoimmune atrophic gastritis (AAG) and are associated with elevated plasma gastrin. Endogenous gastrin autoantibodies have not been described to date. The aim of this study was to investigate the occurrence of autoantibodies to gastrin. Plasma from 50,000 patients, including more than 2000 with AAG, was tested. Gastrin was measured by radioimmunoassay (RIA) in whole plasma and the presence of autoantibody determined by using a control which omitted assay antibody. The quantity and affinity of gastrin autoantibodies was assessed. Three patients had autoantibodies to gastrin. All three had AAG and pernicious anaemia (PA). The antibodies were of low titre and relatively high affinity. Free circulating plasma gastrin levels were within the normal range, but total gastrin levels were elevated. This is the first description of autoantibodies to endogenous gastrin. The incidence of antibodies to gastrin is low, they are found in association with PA, and they may lead to falsely low measurements of plasma gastrin.  (+info)

Associations of anti-beta2-glycoprotein I autoantibodies with HLA class II alleles in three ethnic groups. (5/9574)

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)

The inhibition of myeloperoxidase by ceruloplasmin can be reversed by anti-myeloperoxidase antibodies. (6/9574)

BACKGROUND: The purpose of this study was to characterize the recently reported inhibition of myeloperoxidase (MPO) by ceruloplasmin and to determine whether this may be disturbed in the presence of anti-MPO antibodies. METHODS: Specificity of the binding between ceruloplasmin and MPO was confirmed by Western blotting and enzyme-linked immunosorbent assay (ELISA), and the enzymatic activity of MPO was measured in the presence of ceruloplasmin, affinity-purified anti-MPO antibodies, or both. The affinity of the binding between MPO and ceruloplasmin and MPO and the anti-MPO antibodies was measured using a biosensor, with the results confirmed by chaotrope ELISA. RESULTS: Affinity-purified anti-MPO antibodies from patients with microscopic polyangiitis and florid renal vasculitis inhibited the binding between ceruloplasmin and MPO to a maximum of 72.9 +/- 12.8%, whereas those from patients with Wegener's granulomatosis and only minimal renal involvement inhibited the binding to a maximum of only 36.8 +/- 10.9% (P < 0. 001), with comparable reversal of the ceruloplasmin-mediated inhibition of MPO activity. Measurement of the affinity of the interactions demonstrated that binding between MPO and the anti-MPO antibodies is stronger than that between MPO and ceruloplasmin (1.61 x 107 to 1.33 x 108 vs. 7.46 x 106 m-1), indicating that binding to the autoantibody would be favored in vivo. CONCLUSIONS: This study confirms a role for ceruloplasmin as a physiological inhibitor of MPO, and demonstrates how the inhibition may be disrupted in the presence of anti-MPO antibodies. Because a majority (16 of 21) of the antibodies did not themselves inhibit MPO activity, their interference with the inhibition mediated by ceruloplasmin may be brought about by steric hindrance consequent upon the binding of the antibody to a dominant epitope at or near the active site.  (+info)

Goodpasture antigen: expression of the full-length alpha3(IV) chain of collagen IV and localization of epitopes exclusively to the noncollagenous domain. (7/9574)

BACKGROUND: Tissue injury in Goodpasture (GP) syndrome (rapidly progressive glomerular nephritis and pulmonary hemorrhage) is mediated by antibasement membrane antibodies that are targeted to the alpha3(IV) chain of type IV collagen, one of five alpha(IV) chains that occur in the glomerular basement membrane. GP antibodies are known to bind epitopes within the carboxyl terminal noncollagenous domain (NC1) of the alpha3(IV) chain, termed the GP autoantigen. Whether epitopes also exist in the 1400-residue collagenous domain is unknown because studies to date have focused solely on the NC1 domain. A knowledge of GP epitopes is important for the understanding of the etiology and pathogenesis of the disease and for the development of therapeutic strategies. METHODS: A cDNA construct was prepared for the full-length human alpha3(IV) chain. The construct was stably transfected into human embryonic kidney 293 cells. The purified full-length r-alpha3(IV) chain was characterized by electrophoresis and electron microscopy. The capacity of this chain for binding of GP antibodies from five patients was compared with that of the human r-alpha3(IV)NC1 domain by competitive enzyme-linked immunosorbent assay. RESULTS: The r-alpha3(IV) chain was secreted from 293 cells as a single polypeptide chain that did not spontaneously undergo assembly into a triple-helical molecule. An analysis of GP-antibody binding to the full-length r-alpha3(IV) chain showed binding exclusively to the globular NC1 domain. CONCLUSION: The full-length human alpha3(IV) chain possesses the capacity to bind GP autoantibodies. The epitope(s) is found exclusively on the nontriple-helical NC1 domain of the alpha3(IV) chain, indicating the presence of specific immunogenic properties. The alpha3(IV) chain alone does not spontaneously undergo assembly into a triple-helical homotrimeric molecule, suggesting that coassembly with either the alpha4(IV) and/or the alpha5(IV) chain may be required for triple-helix formation.  (+info)

Identification of a clinically relevant immunodominant region of collagen IV in Goodpasture disease. (8/9574)

BACKGROUND: The characteristic feature of Goodpasture disease is the occurrence of an autoantibody response to the noncollagenous domain of the alpha3 chain of type IV collagen [alpha3(IV)NC1] in the alveolar and glomerular basement membrane. These antibodies are associated with the development of a rapidly progressive glomerulonephritis, with or without lung hemorrhage, whereas autoantibodies specific for the other alpha chains of the heterotrimeric type IV collagen probably do not cause disease. In this study, we have investigated whether differences in fine specificity of autoimmune recognition of the alpha3(IV)NC1 correlate with clinical outcome. METHODS: For mapping of antibody binding to type IV collagen, chimeric collagen constructs were generated in which parts of the alpha3(IV)NC1 domain were replaced by the corresponding sequences of homologous nonreactive alpha1(IV). The different recombinant collagen chimeras allowed the analysis of antibody specificities in 77 sera from well-documented patients. RESULTS: One construct that harbors the aminoterminal third of the alpha3(IV)NC1 was recognized by all sera, indicating that it represents the dominant target of the B-cell response in Goodpasture disease. Seventy percent of the samples recognized other parts of the molecule as well. However, only reactivity to the N-terminus of the alpha3(IV)NC1 correlated with prognosis, that is, kidney survival after six months of follow-up. CONCLUSION: The results indicate the crucial importance of antibody recognition of this particular domain for the pathogenesis of Goodpasture disease, thereby opening new avenues for the development of better diagnostic and therapeutic procedures.  (+info)

Examples of autoimmune diseases include:

1. Rheumatoid arthritis (RA): A condition where the immune system attacks the joints, leading to inflammation, pain, and joint damage.
2. Lupus: A condition where the immune system attacks various body parts, including the skin, joints, and organs.
3. Hashimoto's thyroiditis: A condition where the immune system attacks the thyroid gland, leading to hypothyroidism.
4. Multiple sclerosis (MS): A condition where the immune system attacks the protective covering of nerve fibers in the central nervous system, leading to communication problems between the brain and the rest of the body.
5. Type 1 diabetes: A condition where the immune system attacks the insulin-producing cells in the pancreas, leading to high blood sugar levels.
6. Guillain-Barré syndrome: A condition where the immune system attacks the nerves, leading to muscle weakness and paralysis.
7. Psoriasis: A condition where the immune system attacks the skin, leading to red, scaly patches.
8. Crohn's disease and ulcerative colitis: Conditions where the immune system attacks the digestive tract, leading to inflammation and damage to the gut.
9. Sjögren's syndrome: A condition where the immune system attacks the glands that produce tears and saliva, leading to dry eyes and mouth.
10. Vasculitis: A condition where the immune system attacks the blood vessels, leading to inflammation and damage to the blood vessels.

The symptoms of autoimmune diseases vary depending on the specific disease and the organs or tissues affected. Common symptoms include fatigue, fever, joint pain, skin rashes, and swollen lymph nodes. Treatment for autoimmune diseases typically involves medication to suppress the immune system and reduce inflammation, as well as lifestyle changes such as dietary changes and stress management techniques.

The term "systemic" refers to the fact that the disease affects multiple organ systems, including the skin, joints, kidneys, lungs, and nervous system. LES is a complex condition, and its symptoms can vary widely depending on which organs are affected. Common symptoms include fatigue, fever, joint pain, rashes, and swelling in the extremities.

There are several subtypes of LES, including:

1. Systemic lupus erythematosus (SLE): This is the most common form of the disease, and it can affect anyone, regardless of age or gender.
2. Discoid lupus erythematosus (DLE): This subtype typically affects the skin, causing a red, scaly rash that does not go away.
3. Drug-induced lupus erythematosus: This form of the disease is caused by certain medications, and it usually resolves once the medication is stopped.
4. Neonatal lupus erythematosus: This rare condition affects newborn babies of mothers with SLE, and it can cause liver and heart problems.

There is no cure for LES, but treatment options are available to manage the symptoms and prevent flares. Treatment may include nonsteroidal anti-inflammatory drugs (NSAIDs), corticosteroids, immunosuppressive medications, and antimalarial drugs. In severe cases, hospitalization may be necessary to monitor and treat the disease.

It is important for people with LES to work closely with their healthcare providers to manage their condition and prevent complications. With proper treatment and self-care, many people with LES can lead active and fulfilling lives.

There are several types of pemphigus, including:

1. Pemphigus vulgaris: This is the most common form of the disease and is characterized by the formation of large, painful blisters on the skin and mucous membranes.
2. Pemphigus foliaceus: This type of pemphigus is characterized by the formation of smaller, crusting sores on the skin.
3. Pemphigus erythematosus: This type of pemphigus is characterized by the formation of flat, red sores on the skin.
4. Bullous pemphigoid: This is a rare form of pemphigus that is characterized by the formation of large, fluid-filled blisters on the skin.

Treatment for pemphigus typically involves the use of corticosteroids and immunosuppressive drugs to reduce inflammation and suppress the immune system. In severe cases, hospitalization may be necessary to manage complications such as infection and fluid loss.

Prevention of pemphigus is difficult, but avoiding exposure to known triggers such as certain medications and taking steps to maintain good skin care can help reduce the risk of developing the disease. Early diagnosis and treatment are important to prevent complications and improve outcomes for patients with pemphigus.

A group of autoimmune blistering diseases that are characterized by the formation of large, tense bullae on the skin and mucous membranes. These diseases are caused by abnormal immunological responses to certain antigens, which lead to the production of autoantibodies that attack the basement membrane zone of the skin and mucous membranes, causing damage and blister formation.

There are several types of pemphigoid, bullous diseases, including:

* Pemphigoid, benign chronic
* Pemphigoid, severe
* Bullous pemphigoid
* Epidermolysis bullosa acquisita

Symptoms of pemphigoid, bullous diseases may include:

* Blisters on the skin and mucous membranes
* Redness and swelling around the blisters
* Itching or pain
* Fever

Diagnosis of pemphigoid, bullous diseases is based on a combination of clinical findings, laboratory tests, and biopsy. Treatment involves the use of corticosteroids, immunosuppressive drugs, and antibiotics to manage symptoms and prevent complications.

There are two main types of systemic scleroderma: diffuse cutaneous systemic sclerosis (DCSS) and limited cutaneous systemic sclerosis (LCSS). DCSS is characterized by skin thickening and scar formation over the trunk, arms, and legs, while LCSS is characterized by skin tightening and patches of scaly skin on the hands and face.

The symptoms of systemic scleroderma can include:

* Skin hardening and tightening
* Fatigue
* Joint pain and stiffness
* Muscle weakness
* Swallowing difficulties
* Heartburn and acid reflux
* Shortness of breath
* Raynaud's phenomenon (pale or blue-colored fingers and toes in response to cold temperatures or stress)

The exact cause of systemic scleroderma is not known, but it is believed to involve a combination of genetic and environmental factors. Treatment options for systemic scleroderma include medications to manage symptoms such as pain, stiffness, and swallowing difficulties, as well as physical therapy and lifestyle modifications to improve quality of life.

In summary, systemic scleroderma is a chronic autoimmune disease that affects multiple systems in the body, causing skin hardening and thickening, fatigue, joint pain, and other symptoms. While there is no cure for systemic scleroderma, treatment options are available to manage symptoms and improve quality of life.

Sjögren's syndrome can affect people of all ages, but it most commonly occurs in women between the ages of 40 and 60. The exact cause of the disorder is not known, but it is believed to be an autoimmune response, meaning that the immune system mistakenly attacks the glands as if they were foreign substances.

Symptoms of Sjögren's syndrome can vary in severity and may include:

* Dry mouth (xerostomia)
* Dry eyes (dry eye syndrome)
* Fatigue
* Joint pain
* Swollen lymph nodes
* Rash
* Sores on the skin
* Numbness or tingling in the hands and feet
* Sexual dysfunction

There is no cure for Sjögren's syndrome, but various treatments can help manage the symptoms. These may include:

* Medications to stimulate saliva production
* Eye drops to moisturize the eyes
* Mouthwashes to stimulate saliva production
* Pain relief medication for joint pain
* Anti-inflammatory medication to reduce swelling
* Immunosuppressive medication to suppress the immune system
* Hormone replacement therapy (HRT) to treat hormonal imbalances.

Sjögren's syndrome can also increase the risk of developing other autoimmune disorders, such as rheumatoid arthritis or lupus. It is important for people with Sjögren's syndrome to work closely with their healthcare provider to manage their symptoms and monitor their condition over time.

The symptoms of lupus vulgaris typically include:

* Rough, scaly patches on the skin that may be dark red or purple in color
* Itching or burning sensation on the skin
* Skin thickening or hardening
* Painless ulcers or sores on the skin
* Swollen lymph nodes
* Fever
* Headache
* Joint pain or swelling

The diagnosis of lupus vulgaris is based on a combination of clinical findings and laboratory tests. A physical examination of the skin and mucous membranes can reveal characteristic signs of the condition, such as scaly patches or ulcers. Laboratory tests, such as blood tests or biopsies, may be performed to confirm the diagnosis and rule out other conditions.

Treatment of lupus vulgaris typically involves antibiotics, which can help to clear the infection and reduce symptoms. In severe cases, surgical debridement or laser therapy may be necessary to remove damaged tissue and promote healing. In addition, patients with lupus vulgaris may require supportive care to manage symptoms such as pain, itching, and swelling.

Overall, lupus vulgaris is a chronic skin condition that can cause significant discomfort and disfigurement if left untreated. It is important for individuals in regions where the condition is common to be aware of the signs and symptoms and seek medical attention if they suspect they may have the condition. With proper diagnosis and treatment, however, most patients with lupus vulgaris can experience significant improvement in their symptoms and quality of life.

Autoimmune hemolytic anemia (AIHA) is a specific type of hemolytic anemia that occurs when the immune system mistakenly attacks and destroys red blood cells. This can happen due to various underlying causes such as infections, certain medications, and some types of cancer.

In autoimmune hemolytic anemia, the immune system produces antibodies that coat the surface of red blood cells and mark them for destruction by other immune cells called complement proteins. This leads to the premature destruction of red blood cells in the spleen, liver, and other organs.

Symptoms of autoimmune hemolytic anemia can include fatigue, weakness, shortness of breath, jaundice (yellowing of the skin and eyes), dark urine, and a pale or yellowish complexion. Treatment options for AIHA depend on the underlying cause of the disorder, but may include medications to suppress the immune system, plasmapheresis to remove antibodies from the blood, and in severe cases, splenectomy (removal of the spleen) or bone marrow transplantation.

In summary, autoimmune hemolytic anemia is a type of hemolytic anemia that occurs when the immune system mistakenly attacks and destroys red blood cells, leading to premature destruction of red blood cells and various symptoms such as fatigue, weakness, and jaundice. Treatment options depend on the underlying cause of the disorder and may include medications, plasmapheresis, and in severe cases, splenectomy or bone marrow transplantation.

There are several types of lupus nephritis, each with its own unique characteristics and symptoms. The most common forms include:

* Class I (mesangial proliferative glomerulonephritis): This type is characterized by the growth of abnormal cells in the glomeruli (blood-filtering units of the kidneys).
* Class II (active lupus nephritis): This type is characterized by widespread inflammation and damage to the kidneys, with or without the presence of antibodies.
* Class III (focal lupus nephritis): This type is characterized by localized inflammation in certain areas of the kidneys.
* Class IV (lupus nephritis with crescentic glomerulonephritis): This type is characterized by widespread inflammation and damage to the kidneys, with crescent-shaped tissue growth in the glomeruli.
* Class V (lupus nephritis with sclerotic changes): This type is characterized by hardening and shrinkage of the glomeruli due to scarring.

Lupus Nephritis can cause a range of symptoms, including:

* Proteinuria (excess protein in the urine)
* Hematuria (blood in the urine)
* Reduced kidney function
* Swelling (edema)
* Fatigue
* Fever
* Joint pain

Lupus Nephritis can be diagnosed through a combination of physical examination, medical history, laboratory tests, and kidney biopsy. Treatment options for lupus nephritis include medications to suppress the immune system, control inflammation, and prevent further damage to the kidneys. In severe cases, dialysis or a kidney transplant may be necessary.

1. Polymyositis: This is an inflammatory disease that affects the muscles and can cause muscle weakness, pain, and stiffness.
2. Dercum's disease: This is a rare condition that causes fatty degeneration of the muscles, leading to muscle pain, weakness, and wasting.
3. Inflammatory myopathy: This is a group of conditions that cause inflammation in the muscles, leading to muscle weakness and pain.
4. Dermatomyositis: This is an inflammatory condition that affects both the skin and the muscles, causing skin rashes and muscle weakness.
5. Juvenile myositis: This is a rare condition that affects children and can cause muscle weakness, pain, and stiffness.

The symptoms of myositis can vary depending on the type of condition and its severity. Common symptoms include muscle weakness, muscle pain, stiffness, and fatigue. Other symptoms may include skin rashes, fever, and joint pain.

The diagnosis of myositis typically involves a combination of physical examination, medical history, and laboratory tests such as blood tests and muscle biopsies. Treatment for myositis depends on the underlying cause and may include medications such as corticosteroids, immunosuppressive drugs, and physical therapy. In some cases, surgery may be necessary to remove affected muscle tissue.

Symptoms of type 1 diabetes can include increased thirst and urination, blurred vision, fatigue, weight loss, and skin infections. If left untreated, type 1 diabetes can lead to serious complications such as kidney damage, nerve damage, and blindness.

Type 1 diabetes is diagnosed through a combination of physical examination, medical history, and laboratory tests such as blood glucose measurements and autoantibody tests. Treatment typically involves insulin therapy, which can be administered via injections or an insulin pump, as well as regular monitoring of blood glucose levels and appropriate lifestyle modifications such as a healthy diet and regular exercise.

The symptoms of dermatomyositis can vary in severity and may include:

* Rashes and lesions on the skin, particularly on the face, neck, and hands
* Muscle weakness and fatigue
* Joint pain and stiffness
* Swelling and redness in the affected areas
* Fever
* Headaches
* Fatigue

Dermatomyositis is often associated with other autoimmune disorders, such as polymyositis, and can be triggered by certain medications or infections. There is no cure for dermatomyositis, but treatment options are available to manage the symptoms and prevent complications. Treatment may include medications such as corticosteroids, immunosuppressive drugs, and physical therapy to maintain muscle strength and flexibility.

The term "dermatomyositis" is derived from the Greek words "derma," meaning skin, "myo," meaning muscle, and "-itis," indicating inflammation. The condition was first described in the medical literature in the early 20th century, and since then has been studied extensively to better understand its causes and develop effective treatments.

In summary, dermatomyositis is a rare autoimmune disease that affects both the skin and muscles, causing inflammation and various symptoms such as rashes, weakness, and joint pain. While there is no cure for the condition, treatment options are available to manage the symptoms and prevent complications.

The term "paraneoplastic" refers to the fact that these conditions are parallel to, or associated with, neoplasms (abnormal growths) in the body. The exact cause of paraneoplastic syndromes is not fully understood, but they are believed to be related to the immune system's response to cancer cells.

Some common features of paraneoplastic syndromes include:

1. Autoantibodies: The immune system produces antibodies that attack the body's own tissues and organs.
2. Inflammation: The immune system causes inflammation in various parts of the body.
3. Nerve damage: Paraneoplastic syndromes can affect the nerves, leading to symptoms such as numbness, weakness, and pain.
4. Muscle weakness: Some paraneoplastic syndromes can cause muscle weakness and wasting.
5. Skin rashes: Some patients with paraneoplastic syndromes may develop skin rashes or lesions.
6. Eye problems: Paraneoplastic syndromes can affect the eyes, leading to symptoms such as double vision, blindness, and eye pain.
7. Endocrine dysfunction: Some paraneoplastic syndromes can disrupt the normal functioning of the endocrine system, leading to hormonal imbalances.

Examples of paraneoplastic syndromes include:

1. Lambert-Eaton myasthenic syndrome (LEMS): This is a rare autoimmune disorder that affects the nerves and muscles, leading to muscle weakness and fatigue. It is often associated with small cell lung cancer.
2. Anti-NMDA receptor encephalitis: This is a severe autoimmune disorder that affects the brain and can cause symptoms such as seizures, confusion, and memory loss. It is often associated with ovarian teratoma.
3. Paraneoplastic cerebellar degeneration (PCD): This is a rare condition that affects the cerebellum and can cause symptoms such as coordination problems, balance difficulties, and difficulty with movement. It is often associated with lung cancer or other types of cancer.
4. Stiff-person syndrome: This is a rare autoimmune disorder that affects the central nervous system and can cause symptoms such as muscle stiffness, spasms, and autonomy dysfunction. It is often associated with ovarian teratoma.
5. Polymyositis: This is a rare inflammatory condition that affects the muscles and can cause muscle weakness and wasting. It is often associated with cancer, particularly lung cancer.
6. Dercum's disease: This is a rare condition that affects the adipose tissue and can cause symptoms such as pain, swelling, and limited mobility. It is often associated with cancer, particularly breast cancer.
7. Multiple myeloma: This is a type of cancer that affects the plasma cells in the bone marrow and can cause symptoms such as bone pain, fatigue, and weakness. It is often associated with ovarian teratoma.
8. Painless thyroiditis: This is a rare condition that affects the thyroid gland and can cause symptoms such as thyroid gland inflammation, fatigue, and weight gain. It is often associated with cancer, particularly breast cancer.
9. Ovarian cysts: These are fluid-filled sacs that form on the ovaries and can cause symptoms such as pelvic pain, bloating, and irregular menstrual periods. They are often associated with ovarian teratoma.
10. Endometriosis: This is a condition in which tissue similar to the lining of the uterus grows outside of the uterus and can cause symptoms such as pelvic pain, heavy menstrual bleeding, and infertility. It is often associated with ovarian teratoma.

It's important to note that these conditions are rare and not all cases of ovarian teratoma are associated with them. If you suspect you may have ovarian teratoma, it's important to talk to your healthcare provider for proper diagnosis and treatment.

There are several symptoms of RA, including:

1. Joint pain and stiffness, especially in the hands and feet
2. Swollen and warm joints
3. Redness and tenderness in the affected areas
4. Fatigue, fever, and loss of appetite
5. Loss of range of motion in the affected joints
6. Firm bumps of tissue under the skin (rheumatoid nodules)

RA can be diagnosed through a combination of physical examination, medical history, blood tests, and imaging studies such as X-rays or ultrasound. Treatment typically involves a combination of medications, including nonsteroidal anti-inflammatory drugs (NSAIDs), disease-modifying anti-rheumatic drugs (DMARDs), and biologic agents. Lifestyle modifications such as exercise and physical therapy can also be helpful in managing symptoms and improving quality of life.

There is no cure for RA, but early diagnosis and aggressive treatment can help to slow the progression of the disease and reduce symptoms. With proper management, many people with RA are able to lead active and fulfilling lives.

Grave's disease is the most common cause of hyperthyroidism and affects about 1 in 200 people. It can occur at any age but is more common in women and tends to run in families. The exact cause of Grave's disease is not known, but it may be related to a combination of genetic and environmental factors.

Symptoms of Grave's disease can vary from person to person, but common signs include:

* Weight loss
* Nervousness or anxiety
* Irregular heartbeat (palpitations)
* Increased sweating
* Heat intolerance
* Fatigue
* Changes in menstrual cycle in women
* Enlargement of the thyroid gland, known as a goiter
* Bulging eyes (exophthalmos)

Grave's disease can be diagnosed through blood tests and scans. Treatment options include medication to reduce the production of thyroxine, radioactive iodine therapy to destroy part of the thyroid gland, and surgery to remove part or all of the thyroid gland.

It is important to seek medical attention if you experience any symptoms of Grave's disease, as untreated hyperthyroidism can lead to complications such as heart problems, osteoporosis, and eye problems. With proper treatment, most people with Grave's disease can manage their symptoms and lead a normal life.

The term "polyendocrinopathy" refers to the involvement of multiple endocrine glands, while "autoimmune" indicates that the disorder is caused by an abnormal immune response against the body's own tissues.

Examples of polyendocrinopathies, autoimmune include:

1. Type 1 diabetes with thyroiditis and adrenal insufficiency
2. Hashimoto's thyroiditis with hypophyseal and adrenal involvement
3. Addison's disease with hypothyroidism and hemolytic anemia
4. Autoimmune polyglandular syndrome type 1 (APS-1) with autoantibodies against multiple endocrine glands
5. Autoimmune polyglandular syndrome type 2 (APS-2) with autoantibodies against thyroid, adrenal, and gonadal glands.

The exact cause of polyendocrinopathies, autoimmune is not fully understood, but it is thought to involve a combination of genetic and environmental factors that trigger an abnormal immune response against endocrine tissues. Treatment varies depending on the specific disorder and may include hormone replacement therapy, immunosuppressive medications, and management of associated symptoms.

1. Bullous pemphigoid: This is a rare autoimmune disease that causes large, fluid-filled blisters to form on the skin.
2. Pemphigus: This is another group of rare autoimmune diseases that cause blisters and sores to form on the skin.
3. Impetigo: This is a highly contagious bacterial infection that causes red sores or blisters to form on the skin, often around the nose and mouth.
4. Herpes simplex: This is a viral infection that causes small, painful blisters to form on the skin, often around the mouth or genitals.
5. Molluscum contagiosum: This is a viral infection that causes small, firm bumps to form on the skin, which can become inflamed and itchy.

These conditions can be diagnosed through a combination of physical examination, medical history, and diagnostic tests such as biopsies or blood tests. Treatment for skin diseases, vesiculobullous depends on the underlying cause and may include antibiotics, anti-inflammatory medications, or immunosuppressive drugs. In some cases, surgical removal of the blisters or sores may be necessary. It is important to seek medical attention if you suspect you have a skin disease, vesiculobullous, as these conditions can be difficult to diagnose and treat, and can lead to complications such as infection or scarring.

The exact cause of SPS is not known, but it is believed to be an autoimmune disorder that results in the immune system attacking healthy brain cells, leading to inflammation and damage to the nervous system. Treatment options are limited, and current therapies focus on managing symptoms and improving quality of life.

The definition of Stiff-Person Syndrome (SPS) in the medical field includes:

1. A rare and progressive neurological disorder characterized by muscle stiffness, rigidity, and spasms.
2. Associated with heightened sensitivity to external stimuli such as noise, touch, or emotional stress.
3. Cognitive impairment, anxiety, and depression are common features.
4. Believed to be an autoimmune disorder, causing inflammation and damage to the nervous system.
5. Limited treatment options, with a focus on managing symptoms and improving quality of life.

Polymyositis can affect people of all ages, but it most commonly occurs in adults between the ages of 30 and 60. It is more common in women than men, and the symptoms can vary in severity. The disease may be acute or chronic, and it can affect one or more muscle groups.

The symptoms of polymyositis include:

* Muscle weakness and fatigue
* Pain in the affected muscles
* Wasting of the affected muscles
* Difficulty swallowing (in severe cases)
* Shortness of breath (in severe cases)

The diagnosis of polymyositis is based on a combination of clinical findings, laboratory tests, and imaging studies. Laboratory tests may include blood tests to check for muscle enzymes and inflammatory markers, such as erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP). Imaging studies, such as magnetic resonance imaging (MRI), can help to confirm the diagnosis and assess the extent of the disease.

There is no cure for polymyositis, but treatment can help to manage the symptoms and slow the progression of the disease. Treatment options may include:

* Corticosteroids to reduce inflammation
* Immunosuppressive drugs to suppress the immune system
* Physical therapy to maintain muscle strength and function
* Pain management with analgesics and other medications
* Plasmapheresis to remove antibodies from the blood

The prognosis for polymyositis varies, depending on the severity of the disease and the response to treatment. In general, the prognosis is better for patients who have a mild form of the disease and who respond well to treatment. However, in severe cases, the disease can be life-threatening, and mortality rates are estimated to be as high as 20% to 30%.

There are several types of vasculitis, each with its own set of symptoms and characteristics. Some common forms of vasculitis include:

1. Giant cell arteritis: This is the most common form of vasculitis, and it affects the large arteries in the head, neck, and arms. Symptoms include fever, fatigue, muscle aches, and loss of appetite.
2. Takayasu arteritis: This type of vasculitis affects the aorta and its major branches, leading to inflammation in the blood vessels that supply the heart, brain, and other vital organs. Symptoms include fever, fatigue, chest pain, and shortness of breath.
3. Polymyalgia rheumatica: This is an inflammatory condition that affects the muscles and joints, as well as the blood vessels. It often occurs in people over the age of 50 and is frequently associated with giant cell arteritis. Symptoms include pain and stiffness in the shoulders, hips, and other joints, as well as fatigue and fever.
4. Kawasaki disease: This is a rare condition that affects children under the age of 5, causing inflammation in the blood vessels that supply the heart and other organs. Symptoms include high fever, rash, swollen lymph nodes, and irritability.

The exact cause of vasculitis is not fully understood, but it is thought to be an autoimmune disorder, meaning that the body's immune system mistakenly attacks its own blood vessels. Genetic factors may also play a role in some cases.

Diagnosis of vasculitis typically involves a combination of physical examination, medical history, and diagnostic tests such as blood tests, imaging studies (e.g., MRI or CT scans), and biopsies. Treatment options vary depending on the specific type of vasculitis and its severity, but may include medications to reduce inflammation and suppress the immune system, as well as lifestyle modifications such as exercise and stress management techniques. In severe cases, surgery or organ transplantation may be necessary.

In addition to these specific types of vasculitis, there are other conditions that can cause similar symptoms and may be included in the differential diagnosis, such as:

1. Rheumatoid arthritis (RA): This is a chronic autoimmune disorder that affects the joints and can cause inflammation in blood vessels.
2. Systemic lupus erythematosus (SLE): This is another autoimmune disorder that can affect multiple systems, including the skin, joints, and blood vessels.
3. Polyarteritis nodosa: This is a condition that causes inflammation of the blood vessels, often in association with hepatitis B or C infection.
4. Takayasu arteritis: This is a rare condition that affects the aorta and its branches, causing inflammation and narrowing of the blood vessels.
5. Giant cell arteritis: This is a condition that causes inflammation of the large and medium-sized blood vessels, often in association with polymyalgia rheumatica (PMR).
6. Kawasaki disease: This is a rare condition that affects children, causing inflammation of the blood vessels and potential heart complications.
7. Henoch-Schönlein purpura: This is a rare condition that causes inflammation of the blood vessels in the skin, joints, and gastrointestinal tract.
8. IgG4-related disease: This is a condition that can affect various organs, including the pancreas, bile ducts, and blood vessels, causing inflammation and potentially leading to fibrosis or tumor formation.

It is important to note that these conditions may have similar symptoms and signs as vasculitis, but they are distinct entities with different causes and treatment approaches. A thorough diagnostic evaluation, including laboratory tests and imaging studies, is essential to determine the specific diagnosis and develop an appropriate treatment plan.

The condition is often caused by gallstones or other blockages that prevent the normal flow of bile from the liver to the small intestine. Over time, the scarring can lead to the formation of cirrhosis, which is characterized by the replacement of healthy liver tissue with scar tissue.

Symptoms of liver cirrhosis, biliary may include:

* Jaundice (yellowing of the skin and eyes)
* Itching
* Fatigue
* Abdominal pain
* Dark urine
* Pale stools

The diagnosis of liver cirrhosis, biliary is typically made through a combination of physical examination, medical history, and diagnostic tests such as ultrasound, CT scans, and blood tests.

Treatment for liver cirrhosis, biliary depends on the underlying cause of the condition. In some cases, surgery may be necessary to remove gallstones or repair damaged bile ducts. Medications such as antioxidants and anti-inflammatory drugs may also be prescribed to help manage symptoms and slow the progression of the disease. In severe cases, a liver transplant may be necessary.

Prognosis for liver cirrhosis, biliary is generally poor, as the condition can lead to complications such as liver failure, infection, and cancer. However, with early diagnosis and appropriate treatment, it is possible to manage the symptoms and slow the progression of the disease.

Some common types of connective tissue diseases include:

1. Rheumatoid arthritis (RA): A chronic autoimmune disorder that causes inflammation and joint damage.
2. Systemic lupus erythematosus (SLE): An autoimmune disorder that can affect multiple systems in the body, including the skin, joints, and kidneys.
3. Sjogren's syndrome: An autoimmune disorder that causes dry eyes and mouth, as well as joint pain and swelling.
4. Fibromyalgia: A chronic condition characterized by widespread muscle pain and fatigue.
5. Myositis: Inflammatory diseases that affect the muscles, such as dermatomyositis and polymyositis.
6. Giant cell arteritis: A condition that causes inflammation of the blood vessels, particularly in the head and neck.
7. Takayasu arteritis: A condition that causes inflammation of the blood vessels in the aorta and its branches.
8. Polyarteritis nodosa: A condition that causes inflammation of the blood vessels, particularly in the hands and feet.
9. IgG4-related disease: A condition characterized by inflammation and damage to various organs, including the pancreas, salivary glands, and liver.

Connective tissue diseases can cause a wide range of symptoms, including joint pain and stiffness, fatigue, skin rashes, fever, and weight loss. Treatment options vary depending on the specific disease and its severity, but may include medications such as nonsteroidal anti-inflammatory drugs (NSAIDs), corticosteroids, and disease-modifying anti-rheumatic drugs (DMARDs). In some cases, surgery or physical therapy may also be necessary.

The exact cause of autoimmune hepatitis is not fully understood, but it is believed to involve a combination of genetic and environmental factors. The condition can occur in people of all ages, although it is most common in women between the ages of 20 and 40.

Symptoms of autoimmune hepatitis may include fatigue, loss of appetite, nausea, vomiting, abdominal pain, dark urine, pale stools, and yellowing of the skin and eyes (jaundice). If left untreated, the condition can lead to liver failure and even death.

Treatment for autoimmune hepatitis typically involves medications to suppress the immune system and reduce inflammation in the liver. In severe cases, a liver transplant may be necessary. Early diagnosis and treatment can improve the chances of a successful outcome.

The exact cause of MCTD is not known, but it is believed to be an autoimmune disorder, meaning that the immune system mistakenly attacks healthy tissues in the body. The disease is more common in women than men and typically affects people between the ages of 20 and 50.

Symptoms of MCTD can vary widely and may include:

* Skin rashes or lesions
* Joint pain and stiffness
* Fatigue
* Fever
* Raynaud's phenomenon (digits turn white or blue in response to cold or stress)
* Swollen lymph nodes
* Shortness of breath
* Chest pain
* Abdominal pain
* Weakness and wasting of muscles

There is no cure for MCTD, but treatment focuses on managing symptoms and preventing complications. Medications such as nonsteroidal anti-inflammatory drugs (NSAIDs), corticosteroids, and immunosuppressive drugs may be used to reduce inflammation and suppress the immune system. Physical therapy and exercise may also be helpful in maintaining joint mobility and strength.

The prognosis for MCTD varies depending on the severity of the disease and the presence of certain complications, such as lung or heart involvement. Some people with MCTD may experience a gradual worsening of symptoms over time, while others may experience periods of remission. With appropriate treatment, many people with MCTD are able to manage their symptoms and lead active lives.

Blisters are caused by friction or rubbing against a surface, which causes the top layer of skin to separate from the underlying layer. This separation creates a space that fills with fluid, forming a blister. Blisters can also be caused by burns, chemical exposure, or other types of injury.

There are different types of blisters, including:

1. Friction blisters: These are the most common type of blister and are caused by friction or rubbing against a surface. They are often seen on the hands, feet, and buttocks.
2. Burn blisters: These are caused by burns and can be more severe than friction blisters.
3. Chemical blisters: These are caused by exposure to chemicals and can be very painful.
4. Blisters caused by medical conditions: Certain medical conditions, such as epidermolysis bullosa (a genetic disorder that affects the skin), can cause blisters to form easily.

Blisters can be treated in several ways, depending on their size and location. Small blisters may not require treatment and can heal on their own within a few days. Larger blisters may need to be drained and covered with a bandage to prevent infection. In severe cases, surgical intervention may be necessary.

Preventing blisters is key to avoiding the discomfort and pain they can cause. To prevent blisters, it is important to:

1. Wear properly fitting shoes and clothing to reduce friction.
2. Use lubricating creams or powders to reduce friction.
3. Take regular breaks to rest and allow the skin to recover.
4. Avoid using harsh chemicals or detergents that can cause irritation.
5. Keep the affected area clean and dry to prevent infection.

In conclusion, blisters are a common and uncomfortable condition that can be caused by a variety of factors. While they can be treated and managed, prevention is key to avoiding the discomfort and pain they can cause. By taking steps to prevent blisters and seeking medical attention if they do occur, individuals can reduce their risk of developing this uncomfortable condition.

The symptoms of EBA can vary in severity and may include:

* Blisters and sores on the skin and mucous membranes
* Skin thickening and scarring
* Pain and discomfort
* Infection and inflammation

The exact cause of EBA is not known, but it is believed to be an autoimmune response, where the body's immune system mistakenly attacks its own tissues. Genetic factors may also play a role in the development of EBA.

There is no cure for EBA, but treatment options include:

* Immunosuppressive medications to reduce inflammation and suppress the immune system
* Topical and oral medications to manage pain and prevent infection
* Wound care and debridement to promote healing and reduce scarring
* Phototherapy to reduce inflammation and promote healing

The diagnosis of EBA is based on a combination of clinical findings, laboratory tests, and skin biopsy. Laboratory tests may include:

* Immunofluorescence to detect the presence of autoantibodies against the basement membrane zone
* Direct immunofluorescence to detect the presence of autoantibodies on the skin
* Indirect immunofluorescence to detect the presence of autoantibodies in the blood

The prognosis for EBA is generally poor, with a high risk of complications and a significant impact on quality of life. However, with appropriate treatment, some patients may experience improved symptoms and reduced inflammation. Early diagnosis and aggressive treatment are important to improve outcomes in patients with EBA.

1. Hypothyroidism: This is a condition where the thyroid gland does not produce enough thyroid hormones. Symptoms can include fatigue, weight gain, dry skin, constipation, and depression.
2. Hyperthyroidism: This is a condition where the thyroid gland produces too much thyroid hormone. Symptoms can include weight loss, anxiety, tremors, and an irregular heartbeat.
3. Thyroid nodules: These are abnormal growths on the thyroid gland that can be benign or cancerous.
4. Thyroid cancer: This is a type of cancer that affects the thyroid gland. There are several types of thyroid cancer, including papillary, follicular, and medullary thyroid cancer.
5. Goiter: This is an enlargement of the thyroid gland that can be caused by a variety of factors, including hypothyroidism, hyperthyroidism, and thyroid nodules.
6. Thyrotoxicosis: This is a condition where the thyroid gland produces too much thyroid hormone, leading to symptoms such as weight loss, anxiety, tremors, and an irregular heartbeat.
7. Thyroiditis: This is an inflammation of the thyroid gland that can cause symptoms such as pain, swelling, and difficulty swallowing.
8. Congenital hypothyroidism: This is a condition where a baby is born without a functioning thyroid gland or with a gland that does not produce enough thyroid hormones.
9. Thyroid cancer in children: This is a type of cancer that affects children and teenagers, usually in the form of papillary or follicular thyroid cancer.
10. Thyroid storm: This is a life-threatening condition where the thyroid gland produces an excessive amount of thyroid hormones, leading to symptoms such as fever, rapid heartbeat, and cardiac arrest.

These are just a few examples of the many conditions that can affect the thyroid gland. It's important to be aware of these conditions and seek medical attention if you experience any symptoms or concerns related to your thyroid health.

Causes: Thyroiditis can be caused by a viral or bacterial infection, autoimmune disorders, or radiation exposure.

Symptoms: Symptoms of thyroiditis may include pain and swelling in the neck, difficulty swallowing, hoarseness, fatigue, weight gain, muscle weakness, and depression.

Types: There are several types of thyroiditis, including subacute thyroiditis, silent thyroiditis, and postpartum thyroiditis.

Diagnosis: Thyroiditis is typically diagnosed through a combination of physical examination, blood tests, and imaging studies such as ultrasound or CT scans.

Treatment: Treatment for thyroiditis usually involves antibiotics to treat any underlying infection, pain relief medication to manage neck swelling and discomfort, and hormone replacement therapy to address hormonal imbalances. In some cases, surgery may be necessary to remove part or all of the affected thyroid gland.

Complications: Untreated thyroiditis can lead to complications such as hypothyroidism (underactive thyroid), hyperthyroidism (overactive thyroid), and thyroid nodules or cancer.

Prevention: Preventing thyroiditis is challenging, but maintaining good overall health, avoiding exposure to radiation, and managing any underlying autoimmune disorders can help reduce the risk of developing the condition.

Prognosis: With proper treatment, most people with thyroiditis experience a full recovery and normalization of thyroid function. However, in some cases, long-term hormone replacement therapy may be necessary to manage persistent hypothyroidism or hyperthyroidism.

The hallmark of anti-GBM disease is the presence of circulating anti-GBM antibodies and immune complexes, which are deposited in the glomeruli and lung alveoli, leading to inflammation and tissue damage. The disease can progress rapidly and lead to ESRD if left untreated.

The symptoms of anti-GBM disease vary depending on the severity of the disease and may include:

* Hematuria (blood in urine)
* Proteinuria (excess protein in urine)
* Reduced kidney function
* Fatigue
* Weight loss
* Shortness of breath
* Cough

The diagnosis of anti-GBM disease is based on a combination of clinical findings, laboratory tests, and kidney biopsy. Laboratory tests may include:

* Detection of anti-GBM antibodies in the blood
* Presence of immune complexes in the urine or lung tissue
* Abnormal liver enzymes
* Low complement levels

Treatment of anti-GBM disease typically involves a combination of steroids, immunosuppressive medications, and plasmapheresis (a process that removes harmful antibodies from the blood). In severe cases, kidney transplantation may be necessary. The prognosis for anti-GBM disease is generally poor, with a five-year survival rate of approximately 50%.

There are two main types of Addison's disease: primary and secondary. Primary Addison's disease is caused by an autoimmune disorder that destroys the adrenal glands, while secondary Addison's disease is caused by a problem with the pituitary gland, which regulates the adrenal glands.

Symptoms of Addison's disease can include fatigue, weakness, weight loss, dehydration, and changes in skin color. Treatment involves replacing the missing hormones with medication and managing symptoms. If left untreated, Addison's disease can be life-threatening.

Specialists who may be involved in treating Addison's disease include endocrinologists, primary care physicians, and surgeons. Treatment options can include medication, hydration therapy, and in some cases, surgery to remove the affected adrenal gland(s).

It is important for individuals with Addison's disease to work closely with their healthcare team to manage their condition and avoid complications. With proper treatment and self-management, most people with Addison's disease can lead active and fulfilling lives.

1. Rheumatoid arthritis (RA): An autoimmune disease that causes inflammation in the joints, leading to pain, stiffness, and swelling.
2. Osteoarthritis (OA): A degenerative condition that occurs when the cartilage in the joints wears down over time, causing pain and stiffness.
3. Psoriatic arthritis (PsA): An inflammatory disease that affects both the skin and joints, often occurring in people with psoriasis.
4. Ankylosing spondylitis (AS): A condition that causes inflammation in the spine and peripheral joints, leading to stiffness and pain.
5. Lupus: An autoimmune disease that can affect multiple systems in the body, including the joints, skin, and kidneys.
6. Juvenile idiopathic arthritis (JIA): A condition that affects children under the age of 16, causing inflammation in the joints and potentially leading to long-term complications.
7. Sjogren's syndrome: An autoimmune disorder that affects the glands that produce tears and saliva, causing dryness in the eyes and mouth.
8. Fibromyalgia: A condition characterized by widespread pain, fatigue, and sleep disturbances.
9. Gout: A type of inflammatory arthritis caused by excessive levels of uric acid in the blood, leading to sudden and severe attacks of joint pain.
10. Osteoporosis: A condition characterized by brittle bones and an increased risk of fractures, often occurring in older adults.

Rheumatic diseases can be challenging to diagnose and treat, as they often involve complex symptoms and a range of possible causes. However, with the help of rheumatology specialists and advanced diagnostic tools, it is possible to manage these conditions effectively and improve quality of life for patients.

The symptoms of glomerulonephritis can vary depending on the underlying cause of the disease, but may include:

* Blood in the urine (hematuria)
* Proteinuria (excess protein in the urine)
* Reduced kidney function
* Swelling in the legs and ankles (edema)
* High blood pressure

Glomerulonephritis can be caused by a variety of factors, including:

* Infections such as staphylococcal or streptococcal infections
* Autoimmune disorders such as lupus or rheumatoid arthritis
* Allergic reactions to certain medications
* Genetic defects
* Certain diseases such as diabetes, high blood pressure, and sickle cell anemia

The diagnosis of glomerulonephritis typically involves a physical examination, medical history, and laboratory tests such as urinalysis, blood tests, and kidney biopsy.

Treatment for glomerulonephritis depends on the underlying cause of the disease and may include:

* Antibiotics to treat infections
* Medications to reduce inflammation and swelling
* Diuretics to reduce fluid buildup in the body
* Immunosuppressive medications to suppress the immune system in cases of autoimmune disorders
* Dialysis in severe cases

The prognosis for glomerulonephritis depends on the underlying cause of the disease and the severity of the inflammation. In some cases, the disease may progress to end-stage renal disease, which requires dialysis or a kidney transplant. With proper treatment, however, many people with glomerulonephritis can experience a good outcome and maintain their kidney function over time.

The primary symptom of PAP is shortness of breath (dyspnea), which can range from mild to severe and may be accompanied by coughing, wheezing, and chest tightness. PAP can also lead to respiratory failure, which can be life-threatening if left untreated.

The diagnosis of PAP is based on a combination of clinical symptoms, physical examination findings, and diagnostic tests such as chest radiographs (X-rays), computed tomography (CT) scans, and lung biopsy. A lung biopsy is the most definitive test for PAP, allowing for the identification of characteristic pathological features such as the accumulation of lipoproteinaceous material within the air spaces of the lungs.

Treatment options for PAP include surgical lung biopsy to obtain a definitive diagnosis and monitor disease progression, chest radiation therapy to reduce symptoms and slow disease progression, and medications such as corticosteroids to modulate the immune system and reduce inflammation. In severe cases, lung transplantation may be necessary.

The prognosis for PAP varies depending on the severity of the disease and response to treatment. With appropriate therapy, many patients with PAP can achieve stabilization of their symptoms and improved lung function. However, some patients may experience recurrent episodes of disease exacerbation and may require long-term management and monitoring.

The symptoms of myasthenia gravis can vary in severity and may include:

* Weakness in the arms and legs
* Fatigue and muscle tiredness
* Difficulty swallowing (dysphagia)
* Difficulty speaking or slurred speech (dysarthria)
* Drooping eyelids (ptosis)
* Double vision (diplopia)
* Weakness in the muscles of the face, arms, and legs

The exact cause of myasthenia gravis is not known, but it is believed to be an autoimmune disorder, meaning that the body's immune system mistakenly attacks healthy tissues. It can also be caused by other medical conditions such as thyroid disease, vitamin deficiencies, or infections.

There is no cure for myasthenia gravis, but there are various treatments available to manage the symptoms and improve quality of life. These include:

* Medications such as corticosteroids, immunosuppressants, and cholinesterase inhibitors
* Plasmapheresis, a procedure that removes harmful antibodies from the blood
* Intravenous immunoglobulin (IVIG), which contains antibodies that can help block the immune system's attack on the nerve-muscle junction
* Surgery to remove the thymus gland, which is believed to play a role in the development of myasthenia gravis

It is important for individuals with myasthenia gravis to work closely with their healthcare provider to manage their symptoms and prevent complications. With proper treatment and self-care, many people with myasthenia gravis are able to lead active and fulfilling lives.

Acantholysis is caused by a variety of factors, including genetic mutations, autoimmune disorders, and exposure to certain medications or chemicals. It can affect any area of the body, but it most commonly occurs on the skin of the face, neck, and hands.

The symptoms of acantholysis can vary depending on the underlying cause of the condition. Common symptoms include:

* Thin, fragile skin that is prone to tearing or breaking
* Formation of small, flat scars or lesions on the skin
* Skin that is sensitive to touch or pressure
* Redness and inflammation around the affected area

Acantholysis can be diagnosed through a combination of physical examination, medical history, and laboratory tests. Treatment for acantholysis depends on the underlying cause of the condition and may include topical medications, oral medications, or injectable treatments. In severe cases, surgery may be necessary to repair damaged skin tissue.

Preventing acantholysis can be challenging, but there are some steps that can help reduce the risk of developing the condition. These include:

* Avoiding exposure to harsh chemicals or medications
* Protecting the skin from excessive sun exposure and using sunscreen when necessary
* Using gentle skincare products and avoiding scrubbing or rubbing the skin excessively
* Managing underlying medical conditions, such as autoimmune disorders or hormonal imbalances, that can contribute to acantholysis.

Overall, acantholysis is a rare and complex condition that requires careful diagnosis and management to prevent complications and improve quality of life for individuals affected by the condition.

1) They share similarities with humans: Many animal species share similar biological and physiological characteristics with humans, making them useful for studying human diseases. For example, mice and rats are often used to study diseases such as diabetes, heart disease, and cancer because they have similar metabolic and cardiovascular systems to humans.

2) They can be genetically manipulated: Animal disease models can be genetically engineered to develop specific diseases or to model human genetic disorders. This allows researchers to study the progression of the disease and test potential treatments in a controlled environment.

3) They can be used to test drugs and therapies: Before new drugs or therapies are tested in humans, they are often first tested in animal models of disease. This allows researchers to assess the safety and efficacy of the treatment before moving on to human clinical trials.

4) They can provide insights into disease mechanisms: Studying disease models in animals can provide valuable insights into the underlying mechanisms of a particular disease. This information can then be used to develop new treatments or improve existing ones.

5) Reduces the need for human testing: Using animal disease models reduces the need for human testing, which can be time-consuming, expensive, and ethically challenging. However, it is important to note that animal models are not perfect substitutes for human subjects, and results obtained from animal studies may not always translate to humans.

6) They can be used to study infectious diseases: Animal disease models can be used to study infectious diseases such as HIV, TB, and malaria. These models allow researchers to understand how the disease is transmitted, how it progresses, and how it responds to treatment.

7) They can be used to study complex diseases: Animal disease models can be used to study complex diseases such as cancer, diabetes, and heart disease. These models allow researchers to understand the underlying mechanisms of the disease and test potential treatments.

8) They are cost-effective: Animal disease models are often less expensive than human clinical trials, making them a cost-effective way to conduct research.

9) They can be used to study drug delivery: Animal disease models can be used to study drug delivery and pharmacokinetics, which is important for developing new drugs and drug delivery systems.

10) They can be used to study aging: Animal disease models can be used to study the aging process and age-related diseases such as Alzheimer's and Parkinson's. This allows researchers to understand how aging contributes to disease and develop potential treatments.

The exact cause of NMO is not known, but it is believed to be an autoimmune disorder, meaning that the immune system mistakenly attacks healthy cells in the body. Genetic and environmental factors may contribute to the development of NMO. The disease is more common in women than men, and typically affects people between the ages of 20 and 50.

The symptoms of NMO can vary widely depending on the location and severity of the inflammation. Common symptoms include:

* Vision loss or blurred vision
* Pain or numbness in the eyes, face, or neck
* Weakness or paralysis of the limbs
* Difficulty walking or maintaining balance
* Bladder or bowel dysfunction
* Fatigue and fever

NMO can be difficult to diagnose, as the symptoms are similar to those of other conditions such as multiple sclerosis. A diagnosis of NMO is typically made based on a combination of clinical findings, laboratory tests, and imaging studies such as MRI or CT scans.

Treatment for NMO typically involves immunosuppressive medications to reduce inflammation and prevent future attacks. In some cases, corticosteroids may be prescribed to reduce swelling in the central nervous system. Plasmapheresis, a process that removes harmful antibodies from the blood, may also be used in some cases. Physical therapy and other supportive measures can help manage the symptoms of NMO and improve quality of life.

Prognosis for NMO varies depending on the severity of the inflammation and the promptness of treatment. In general, early diagnosis and aggressive treatment can lead to a better outcome. However, some individuals with NMO may experience long-term or permanent damage to their optic nerves or other parts of the central nervous system.

There is currently no cure for NMO, but ongoing research is exploring new treatments and therapies that may help improve outcomes for individuals with this condition. With proper treatment and supportive care, many people with NMO are able to manage their symptoms and lead active lives.

The syndrome is typically diagnosed based on the presence of anticardiolipin antibodies (aCL) or lupus anticoagulant in the blood. Treatment for antiphospholipid syndrome may involve medications to prevent blood clots, such as heparin or warfarin, and aspirin or nonsteroidal anti-inflammatory drugs (NSAIDs) to reduce pain and inflammation. In some cases, intravenous immunoglobulin (IVIG) may be given to reduce the levels of antibodies in the blood. Plasmapheresis, a process that removes antibodies from the blood, may also be used in some cases.

Antiphospholipid syndrome is associated with other autoimmune disorders, such as systemic lupus erythematosus (SLE), and may be triggered by certain medications or infections. It is important for individuals with antiphospholipid syndrome to work closely with their healthcare provider to manage their condition and reduce the risk of complications.

The main symptoms of PTI include:

* Purple spots or bruises (purpura) on the skin, which may be caused by minor trauma or injury.
* Thrombocytopenia (low platelet count), typically less than 50,000 platelets/mm3.
* Mild anemia and reticulocytosis (increased immature red blood cells).
* Elevated levels of autoantibodies against platelet membrane glycoproteins (GP) and other platelet proteins.
* No evidence of other causes of thrombocytopenia, such as bone marrow disorders or infections.

The exact cause of PTI is unknown, but it is believed to involve an immune-mediated response triggered by a genetic predisposition. Treatment options for PTI include corticosteroids, intravenous immunoglobulin (IVIG), and splenectomy in severe cases. The prognosis for PTI is generally good, with most patients experiencing resolution of symptoms and normalization of platelet counts within a few months to a year after treatment. However, some individuals may experience recurrent episodes of thrombocytopenia and purpura throughout their lives.

The hallmark of Wegener Granulomatosis is the formation of granulomas, which are clusters of immune cells that form in response to infection or inflammation. In this condition, however, the granulomas are not caused by an infectious agent but rather by the body's own immune system attacking its own tissues.

The symptoms of Wegener Granulomatosis can vary depending on the organs affected and can include:

* Fever
* Joint pain
* Fatigue
* Weight loss
* Shortness of breath
* Chest pain
* Coughing up blood
* Abdominal pain
* Blood in urine or stool
* Headache

The exact cause of Wegener Granulomatosis is not known, but it is believed to involve a combination of genetic and environmental factors. Treatment typically involves the use of corticosteroids and other immunosuppressive medications to reduce inflammation and prevent further damage to the body. In some cases, plasmapheresis (plasma exchange) may also be used to remove harmful antibodies from the blood.

Wegener Granulomatosis is a relatively rare condition, affecting approximately 2-4 people per million each year. It can occur at any age but is most commonly diagnosed in adults between the ages of 40 and 60. With early diagnosis and proper treatment, many people with Wegener Granulomatosis can experience a good outcome and improved quality of life. However, if left untreated, the condition can be fatal.

Symptoms of CNS lupus vasculitis can include headaches, seizures, confusion, weakness or paralysis, vision problems, and changes in personality or behavior. The condition can be difficult to diagnose, as it may mimic other conditions such as stroke, infection, or tumors.

Treatment of CNS lupus vasculitis typically involves high doses of corticosteroids to reduce inflammation and prevent further damage. In severe cases, intravenous immunoglobulin (IVIG) or plasmapheresis may be used to remove harmful antibodies from the blood. Anticoagulation therapy may also be prescribed to prevent blood clots.

While CNS lupus vasculitis can be a life-threatening condition, early diagnosis and aggressive treatment can improve outcomes. However, long-term follow-up is essential to monitor for recurrences of the disease and manage any ongoing neurological symptoms.

The primary symptoms of celiac disease include diarrhea, abdominal pain, fatigue, weight loss, and bloating. However, some people may not experience any symptoms at all, but can still develop complications if the disease is left untreated. These complications can include malnutrition, anemia, osteoporosis, and increased risk of other autoimmune disorders.

The exact cause of celiac disease is unknown, but it is believed to be triggered by a combination of genetic and environmental factors. The disease is more common in people with a family history of celiac disease or other autoimmune disorders. Diagnosis is typically made through a combination of blood tests and intestinal biopsy, and treatment involves a strict gluten-free diet.

Dietary management of celiac disease involves avoiding all sources of gluten, including wheat, barley, rye, and some processed foods that may contain hidden sources of these grains. In some cases, nutritional supplements may be necessary to ensure adequate intake of certain vitamins and minerals.

While there is no known cure for celiac disease, adherence to a strict gluten-free diet can effectively manage the condition and prevent long-term complications. With proper management, people with celiac disease can lead normal, healthy lives.

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714-5. ISBN 978-1-4557-2684-4. American Association for Clinical Chemistry (13 November 2019). "Autoantibodies". Lab Tests ... autoantibodies). All people have different immunology graphs. A 2016 research paper by Metcalf et al., amongst whom were Neil ...
Autoantibodies to glutamate receptor GluR3 in Rasmussen's encephalitis. Science. 1994 Jul 29;265(5172):648-51. Mantegazza R, ... Anti-glutamate receptor antibodies are autoantibodies detected in serum and/or cerebrospinal fluid samples of a variety of ... Mechanisms underlying cerebellar motor deficits due to mGluR1-autoantibodies. Ann Neurol. 2003 Mar;53(3):325-36. During MJ, ... Acute cerebellar ataxia and consecutive cerebellitis produced by glutamate receptor delta2 autoantibody. Brain Dev. 2007 May;29 ...
... s, or PR3-ANCA, or antineutrophil cytoplasmic antibodies, are a type of autoantibody, an antibody produced by the body ...
Konstandoulakis MM, Syrigos KN, Leandros M, Charalabopoulos A, Manouras A, Golematis BC (1998). "Autoantibodies in the serum of ... 2005). "Significance of smooth muscle/anti-actin autoantibodies in celiac disease". Acta Gastroenterol. Latinoam. 35 (2): 83-93 ...
Yehuda Shoenfeld; M. Eric Gershwin; Pier-Luigi Meroni (2007). Autoantibodies. Elsevier. pp. 98-. ISBN 978-0-444-52763-9. ...
"HIS - Clinical: Histone Autoantibodies, Serum". Mayo Medical Laboratories. Retrieved 2018-08-04. (Autoantibodies). ... Muller, Sylviane (2014). Chapter 23 - Histone Autoantibodies, In Autoantibodies (Third ed.). San Diego, CA. p. 195. doi:10.1016 ... Multiple "Autoantibodies" to Cell Constituents in Systematic Lupus Erythematosus. In: Ciba Foundation Symposium - Cellular ... Anti-histone antibodies are autoantibodies that are a subset of the anti-nuclear antibody family, which specifically target ...
Kenneth Michael Pollard (2006). Autoantibodies and autoimmunity: molecular mechanisms in health and disease. Wiley-VCH. pp. 293 ...
Shojania AM, Meilleur G, Alvi AW (1987). "An autoantibody with potent antithrombin activity whose action could be inhibited by ... Shibata S, Sasaki T, Harpel P, Fillit H (1994). "Autoantibodies to vascular heparan sulfate proteoglycan in systemic lupus ... Anti-thrombin antibodies are autoantibodies directed against thrombin that may constitute a fraction of lupus anticoagulant and ...
... (ACAs; often styled solid, anticentromere) are autoantibodies specific to centromere and kinetochore ...
Wesierska-Gadek J, Hohenuer H, Hitchman E, Penner E (1996). "Autoantibodies against nucleoporin p62 constitute a novel marker ...
IgG3 Caspr autoantibodies were found during the acute GBS-like phase, while IgG4 Caspr autoantibodies were present during the ... Autoantibodies to components of the Ranvier nodes, specially autoantibodies the Contactin-associated protein 1 (CASPR), cause a ... Parry and Clarke in 1988 described a neuropathy which was later found to be associated with IgM autoantibodies directed against ... These cases seem to be related to the presence of anti-neurofascin autoantibodies.[citation needed] Chronic inflammatory ...
"Isolation and characterization of cDNA encoding a human nuclear antigen predominantly recognized by autoantibodies from ...
1998). "Autoantibodies against a 210 kDa glycoprotein of the nuclear pore complex as a prognostic marker in patients with ... Courvalin JC, Lassoued K, Worman HJ, Blobel G (1990). "Identification and characterization of autoantibodies against the ... Nickowitz RE, Worman HJ (1993). "Autoantibodies from patients with primary biliary cirrhosis recognize a restricted region ...
Anti-mitochondrial antibodies (AMA) are autoantibodies, consisting of immunoglobulins formed against mitochondria, primarily ... Mitochondrial antigens and autoantibodies: from anti-M1 to anti-M9. Klin Wochenschr 64(19):897-909 Labro MT, Andrieu MC, Weber ...
Auto-antibodies against histones have been reported to be involved. Anti-AQP1 could be involved in atypical MS and NMO N-type ... Anti-neurofascin autoantibodies have been reported in atypical cases of MS and CIDP, and a whole spectrum of Anti-neurofascin ... Some auto-antibodies have been found consistently across different MS cases but there is still no agreement on their relevance ... Other auto-antibodies can be used to stablish a differential diagnosis from very different diseases like Sjögren syndrome which ...
Autoantibodies are also common. Investigators at the National Institute of Allergy and Infectious Diseases at the US National ...
Mallone R, Perin PC (2006). "Anti-CD38 autoantibodies in type? diabetes". Diabetes/Metabolism Research and Reviews. 22 (4): 284 ...
CS1: long volume value, Autoantibodies). ...
Autoantibodies against CD74 have been identified as promising biomarkers in the early diagnosis of the autoimmune disease ... June 2014). "Autoantibodies against CD74 in spondyloarthritis". Annals of the Rheumatic Diseases. 73 (6): 1211-1214. doi: ...
Autoantibodies are usually absent or very low, so instead of being given in standard reference ranges, the values usually ... chronolab.com > Autoantibodies associated with rheumatic diseases > Reference ranges Retrieved on April 29, 2010 "AMA - ...
This is the highest dilution of the serum at which autoantibodies are still detectable. Positive autoantibody titres at a ... Autoantibody screening is useful in the diagnosis of autoimmune disorders and monitoring levels helps to predict the ... In case no defined autoantibody can be detected (e.g. anti-ENA antibodies), the testing of anti-DFS70 antibodies is recommended ... Lyons, R; Narain, S; Nichols, C; Satoh, M; Reeves, WH (June 2005). "Effective use of autoantibody tests in the diagnosis of ...
The presence of autoantibodies against citrullinated proteins in rheumatoid arthritis patients was first described in the mid- ... chronolab.com > Autoantibodies associated with rheumatic diseases > Reference ranges Retrieved on 29 April 2010 Gardette A, ... Subsequent studies demonstrated that autoantibodies from RA patients react with a series of different citrullinated antigens, ... Anti-citrullinated protein antibodies (ACPAs) are autoantibodies (antibodies to an individual's own proteins) that are directed ...
"Antinuclear autoantibodies specific for lamins. Characterization and clinical significance". Ann Intern Med. 108 (6): 829-3. ...
With his colleagues, he was the first to describe smooth muscle reactive autoantibodies and this led the way to important ... cite journal}}: Cite journal requires ,journal= (help) Toh BH (1979). "Smooth muscle autoantibodies and autoantigens". Clin Exp ... he was there he was particularly involved in perfecting the new technique of using immunoflourescence to define autoantibodies ...
This effect can also occur after an infection causes the production of autoantibodies to other structures within the nucleus. ... Subsequently, in 1957, antibodies to dsDNA were the first autoantibodies to be identified in patients with SLE. Although the ... Hueber W, Utz PJ, Steinman L, Robinson WH (2002). "Autoantibody profiling for the study and treatment of autoimmune disease". ... Automated analysis of the well fluorescence allows for rapid detection of autoantibodies. Microarrays are a newly emerging ...
Antineutrophil autoantibodies in Graves' Disease. Implications of thyrotropin binding to neutrophils. J Clin Invest. 1985; 75: ...
... and presence of autoantibodies against several self-structures in the serum and synovial fluid. These autoantibodies ( ... In addition, autoantibodies are proven to be useful disease markers for RA, and different diagnostic tools are being developed ... Recently, a direct link was proposed between the presence of autoantibodies and bone erosion as well as in the induction of ... In this review, the diagnostic value of autoantibodies, their synthesis and function as a mediator of joint inflammation, and ...
... 03/20/2023 ... say they have identified a type of autoantibody that may worsen the condition and have also found how these autoantibodies ... a simple explanation for the differences of anti-DNA antibodies in SLE by demonstrating that some of these autoantibodies have ...
... anti-gephyrin autoantibodies could help identify patients at higher risk for GI symptoms like constipation. ... Systemic Sclerosis Autoantibody Linked to GI Dysfunction Identified for First Time * Autoantibodies Could Help Predict Cancer ... Anti-gephyrin autoantibodies have been tied to lower gastrointestinal (GI) dysfunction, such as severe constipation and ... McMahan and colleagues then investigated the prevalence of the autoantibody by screening the sera of 188 patients with SSc who ...
... Clin Immunol. 2007 Dec;125(3):247-56. doi: ... GWB autoantibodies targeted epitopes that included the N-terminus of Ago2 and the nuclear localization signal (NLS) containing ... and immunoprecipitation of recombinant proteins indicated that autoantibodies in this cohort of anti-GWB sera were directed ... of this study was to identify the target GWB autoantigens reactive with 55 sera from patients with anti-GWB autoantibodies and ...
Chi C-Y, Chu C-C, Liu J-P, Lin C-H, Ho M-W, Lo W-J, Anti-IFN-γ autoantibodies in adults with disseminated nontuberculous ... Browne SK, Zaman R, Sampaio EP, Jutivorakool K, Rosen LB, Ding L, Anti-CD20 (rituximab) therapy for anti-IFN-γ autoantibody- ... Koya T, Tsubata C, Kagamu H, Koyama K, Hayashi M, Kuwabara K, Anti-interferon-gamma autoantibody in a patient with disseminated ... Döffinger R, Helbert MR, Barcenas-Morales G, Yang K, Dupuis S, Ceron-Gutierrez L, Autoantibodies to interferon-gamma in a ...
Avhandling: Complement aberrations and autoantibodies to complement proteins in relation to disease mechanisms. . ... Complement aberrations and autoantibodies to complement proteins in relation to disease mechanisms. Detta är en avhandling från ... The thesis is based on four papers (I-IV). (I and II) Autoantibodies to the C3 cleaving enzyme complex of the alternative ... Nyckelord: MEDICIN; MEDICINE; GM allotypes; C3 nephritic factors; C1q autoantibodies; serum bactericidal activity; Neisseria ...
Our novel association of PLIN1 autoantibodies in the Aire−/− mouse provides a model system to recapitulate autoantibodies in ... An RLBA was adapted for anti-PLIN1 autoantibody screening in humans. By this assay, autoantibodies to PLIN1 were present in ... Due to the fact that autoantibodies commonly precede detection of symptoms, autoantibodies to PLIN1 may provide a useful tool ... Autoantibodies to Perilipin-1 Define a Subset of Acquired Generalized Lipodystrophy Caleigh Mandel-Brehm 0000-0001-7764-6529 ...
Autoantibodies - blood Child Child, Preschool Diabetes Mellitus, Type 1 - blood - immunology Erythrocyte Count Female HLA ... Islet autoantibodies (IAs) precede the clinical onset of type 1 diabetes (T1D); however, the knowledge is limited about whether ... Reduction in White Blood Cell, Neutrophil, and Red Blood Cell Counts Related to Sex, HLA, and Islet Autoantibodies in Swedish ...
Thyroid autoantibodies in women with and without thyroid disorders in an iodine-replete area ... The distribution of autoantibody concentration is shown as box plots (Figures 1 and 2). Median (range) for TPOAb in these ... Thyroid autoantibodies in women with and without thyroid disorders in an iodine-replete area ... Frequency of positive autoantibodies did not increase with age in patients with thyroid disorders or in the control group. ...
Prevalence of laminin 332-specific autoantibodies, detected by a novel enzyme-linked immunosorbent assay, in patients with ... Prevalence of laminin 332-specific autoantibodies, detected by a novel enzyme-linked immunosorbent assay, in patients with ...
Our results indicated that autoantibodies to class A scavenger receptors might contribute to the breakdown of self-tolerance by ... and the functional implication of those autoantibodies in the phagocytic clearance of apoptotic cells by macrophages. Purified ... From: Anti-class a scavenger receptor autoantibodies from systemic lupus erythematosus patients impair phagocytic clearance of ...
Folate receptor autoantibodies and autism... replicated (yet again) ... In short, folate receptor autoantibodies are probably important to at least some autism.. Oh, and while were on the topic of ... Folate receptor autoantibodies are prevalent in children diagnosed with autism spectrum disorder, their normal siblings and ... High milk consumers have an increased risk of folate receptor blocking autoantibody production but this does not affect folate ...
e WT pancreas sections were incubated with serum from either WT or Satb1 cKO animals to detect the presence of autoantibodies ... Detection of autoantibodies. The WT pancreas sample was prepared as previously described. 5 μm thick sections were ... 5d). This translated into the production of autoantibodies (Fig. 5e, Supplementary Fig. 11d) as also previously demonstrated26. ...
N2 - Background: Autoantibodies to zinc transporter 8 (ZnT8A) are usually the last autoantibody specificity to appear in the ... AB - Background: Autoantibodies to zinc transporter 8 (ZnT8A) are usually the last autoantibody specificity to appear in the ... Background: Autoantibodies to zinc transporter 8 (ZnT8A) are usually the last autoantibody specificity to appear in the ... abstract = "Background: Autoantibodies to zinc transporter 8 (ZnT8A) are usually the last autoantibody specificity to appear in ...
... in which functional IgG autoantibodies to IgE or its high‐affinity receptor (FcεRI) induces mast cell degranulation and ...
Sengenics is meeting the need for blood-based biomarkers in neurological disease with autoantibody signature discovery ... Driving discovery of autoantibody biomarkers. Sengenics can help, with solutions to support discovery of biomarker signatures ... 2016) Augmentation of Autoantibodies by Helicobacter pylori in Parkinsons Disease Patients May Be Linked to Greater Severity. ... Autoantibodies make excellent biomarkers in diseases with an inflammatory or autoimmune component. ...
This blood test checks for substances called antibodies. These are made by your body in response to insulin and other chemicals related to insulin. It is used to find out whether you have type 1 or type 2 diabetes.
IgG autoantibody testing of a subsample of stored serum from 2011-2012 cohorts was conducted to estimate the prevalence and ... IgG autoantibody testing of a subsample of stored serum from phase 1 (1988-91) NHANES III participants was conducted to ... Testing of IgG autoantibodies to human cellular antigens was performed by the HEp-2 cell immunofluorescence assay using slides ... Autoantibodies - Immunofluorescence Analyses (Surplus) (SSNH3ANA). Data File: SSNH3ANA.xpt. First Published: August 2019. Last ...
In this paper we investigated 25 SLE-patients for autoantibodies against nucleoporin p62. Nucleoporin p62 autoantibodies have ... Nuclear Pore Protein p62 Autoantibodies in Systemic Lupus Erythematosus Doris M Kraemer*, 1, Hans-Peter Tony2. 1 Queens Cancer ... Autoantibodies in primary biliary cirrhosis are recognizing the amino terminal fragment of p62 [17]. Since the aminoterminal ... Recently several novel autoantibodies against a variety of specific nuclear pore proteins have been described, including the ...
Development of ACE2 autoantibodies after SARS-CoV-2 infection. Arthur, John M; Forrest, J Craig; Boehme, Karl W; Kennedy, ... Development of ACE2 autoantibodies after SARS-CoV-2 infection. ... We hypothesized that autoantibodies against ACE2 may develop ...
Autoantibodies in Atrial Fibrillation-State of the Art. Research output: Contribution to journal › Review article › Academic › ...
It is not known whether the DFS70 autoantibodies are protective or pathogenic. One of the factors suspected of inducing the ... Background: The anti-DFS70 autoantibodies are one of the most commonly and widely described agent of unknown clinical ... Relationship Between Anti-DFS70 Autoantibodies and Oxidative Stress.pdf - Published Version Available under License Creative ... 2022) Relationship Between Anti-DFS70 Autoantibodies and Oxidative Stress. Biomarker Insights, 17. ISSN 1177-2719 ...
title = "Autoantibody panel screening in recurrent miscarriages",. abstract = "Problem: Antiphospholipid autoantibodies (aPL), ... The analysis was also performed with several panels of autoantibodies, each of which contained two or more autoantibodies. ... The analysis was also performed with several panels of autoantibodies, each of which contained two or more autoantibodies. ... The analysis was also performed with several panels of autoantibodies, each of which contained two or more autoantibodies. ...
Detection of igg autoantibodies against dsg1 and dsg3 by elisa. *Detection of igg autoantibodies against dsg2 by in-house elisa ... The production of autoantibodies against Dsg1 and/or Dsg3 was observed in the groups of family members and CTL (Fig. 1B-C). ... Detection of IgG autoantibodies against Dsg2 by in-house ELISA. Briefly, 5 ng/μL of Dsg2 (Leinco, Fenton, USA) diluted in a ... Detection of IgG autoantibodies against Dsg1 and Dsg3 by ELISA. The samples were tested with a commercial ELISA kit (MBL, ...
An update on autoantibodies in systemic lupus erythematosus. Gómez-Bañuelos, Eduardo; Fava, Andrea; Andrade, Felipe ... Scleroderma autoantibodies in guiding monitoring and treatment decisions. Shah, Shivani; Denton, Christopher P. ...
Circulating iso and auto antibodies to human spermatozoa in infertility.. Authors: Mohan, H. Yadav, S. Singh, U. Kadian, A. ... Mohan H, Yadav S, Singh U, Kadian A, Mohan P. Circulating iso and auto antibodies to human spermatozoa in infertility. Indian ...
In conclusion, anti-neutrophil autoantibodies from RA patients recognize different antigens in the cytoplasm and in the nucleus ... The objective of this study was to characterize antigens recognized by neutrophil-specific autoantibodies from patients with RA ... Specificities of anti-neutrophil autoantibodies in patients with rheumatoid arthritis (RA). Brimnes J., Halberg P., Jacobsen S ... The objective of this study was to characterize antigens recognized by neutrophil-specific autoantibodies from patients with RA ...
Neuromyelitis optica: Clinical syndrome and the NMO-IgG autoantibody marker. / Weinshenker, B. G.; Wingerchuk, D. M. Advances ... Weinshenker, B. G. ; Wingerchuk, D. M. / Neuromyelitis optica : Clinical syndrome and the NMO-IgG autoantibody marker. Advances ... A new autoantibody marker called neuromyelitis optica immunoglobulin G (NMO-IgG), which targets the water channel protein ... Weinshenker, B. G., & Wingerchuk, D. M. (2008). Neuromyelitis optica: Clinical syndrome and the NMO-IgG autoantibody marker. In ...
... and anti-lipoprotein auto-antibodies - with risk profiles varying across different types of auto-antibodies (Table 2). ... Cardiovascular Disease in Rheumatoid Arthritis: Risk Factors and the Role of Auto-antibodies. Leticia Ferri1, Grace Crocket 2, ... Four types of auto-antibodies were identified showing association with cardiovascular events -RF, anti-CCP, aPL, ... Figure: 1A PRISMA diagram for review on epidemiology and risk factors; 1B PRISMA diagram for review on auto-antibodies*. ‡ For ...
Elevated Autoantibodies in Subacute Human Spinal Cord Injury Are Naturally Occurring Antibodies.PDF ... Data_Sheet_4_Elevated Autoantibodies in Subacute Human Spinal Cord Injury Are Naturally Occurring Antibodies. .PDF (. 88.12 kB ... Here we show that autoantibodies that increase at the subacute phase of human SCI, 1 month after lesion, are already present in ... The increase of these autoantibodies is a fast phenomenon-their levels are already elevated before 5 days after lesion- ...
  • Rheumatoid arthritis is a systemic, polygenic, and multifactorial syndrome characterized by erosive polyarthritis, damage to joint architecture, and presence of autoantibodies against several self-structures in the serum and synovial fluid. (hindawi.com)
  • In this study, Luciferase Immunoprecipitation Systems (LIPS), a fluid phase immunoassay, was used to analyze SS serum autoantibody responses to 12 recombinant autoantigens in a cohort of 17 healthy volunteers and 72 patients with primary SS. (nih.gov)
  • High prevalence of serum folate receptor autoantibodies in children with autism spectrum disorders. (blogspot.com)
  • Our high-density protein microarray assays and advanced bioinformatics enable highly specific and reproducible detection of disease-relevant autoantibodies directly from patient serum. (sengenics.com)
  • IgG autoantibody testing of a subsample of stored serum from phase 1 (1988-91) NHANES III participants was conducted to estimate the prevalence and specificities of selected autoantibodies in the US population. (cdc.gov)
  • To compare the participation of desmogleins 1, 2 and 3 through the production of serum autoantibodies, and protein and gene expression in the skin/mucosa of patients with pemphigus foliaceus and pemphigus vulgaris. (anaisdedermatologia.org.br)
  • In vitro qualitative detection of autoantibodies against diabetes in human serum provides a reference for the classification, prediction and prevention of diabetes. (szblot.com)
  • In an effort to understand the origin of systemic lupus erythematosus and why some patients present with more severe disease than others, Johns Hopkins Medicine researchers say they have identified a type of autoantibody that may worsen the condition and have also found how these autoantibodies originate. (hopkinsmedicine.org)
  • Additional testing revealed that certain SS patients were also seropositive for autoantibodies classically associated with other autoimmune conditions, including gastric ATPB (autoimmune gastritis), PDCE2 (primary biliary cirrhosis), RNP-A (systemic lupus erythematosus) and CENP-A (systemic sclerosis) and GAD65 (autoimmune encephalitis). (nih.gov)
  • Systemic lupus erythematosus (SLE) is a systemic autoimmune disease which is classically characterised by a variety of autoantibodies to deoxyribonucleic acid (DNA), ribonucleic acid (RNA), other nuclear and cytoplasmic antigens. (openrheumatologyjournal.com)
  • Systemic lupus erythematosus, autoantibodies, nucleoporin p62. (openrheumatologyjournal.com)
  • McMahan and colleagues then investigated the prevalence of the autoantibody by screening the sera of 188 patients with SSc who presented consecutively to the Johns Hopkins Scleroderma Center between April 2016 and August 2017, as well as 40 controls, and compared GI symptom severity between antibody-positive and antibody-negative patients with SSc. (medscape.com)
  • To compare the prevalence of positive autoantibodies in patients with thyroid disorders and healthy subjects in an iodine-replete area of the Islamic Republic of Iran, we studied 930 women in a clinic-based study: 698 patients (286 hypothyroid, 140 hyperthyroid, 272 with simple goitre) and 232 healthy women. (who.int)
  • These autoantibodies (anticitrullinated protein/peptide antibodies (ACPAs), rheumatoid factors (RF), anticollagen type II antibodies, antiglucose-6 phosphate isomerase antibodies, anticarbamylated protein antibodies, and antiacetylated protein antibodies) have different characteristics, diagnostic/prognostic value, and pathological significance in RA patients. (hindawi.com)
  • Our findings provide a simple explanation for the differences of anti-DNA antibodies in SLE by demonstrating that some of these autoantibodies have multiple functions," says corresponding author Felipe Andrade, M.D., Ph.D. , an associate professor of medicine in the Division of Rheumatology at the Johns Hopkins University School of Medicine. (hopkinsmedicine.org)
  • SLE is serologically defined by a variety of autoantibodies including anti-DNA, anti-phospholipid, anti-Sm and other antinuclear antibodies. (openrheumatologyjournal.com)
  • Problem: Antiphospholipid autoantibodies (aPL), antithyroid antibodies and anti-extractable nuclear antigens (anti-ENA) have all been reported to be associated with recurrent miscarriages (RM) and infertility. (biu.ac.il)
  • Materials and Methods: Fifty-eight women with impaired fertility (38 women with RM and 20 women with infertility, but no miscarriages) and 28 control parous women were screened for seven autoantibodies [antithyroglobulin (aTG), antithyroid peroxidase (aTPO), anticardiolipin (aCL), antiphosphatidyl-serine (aPS), antiprothrombin antibodies (aPT), anti-beta 2 glycoprotein 1 (aβ 2 GP1), and anti-ENA]. (biu.ac.il)
  • We hypothesized that autoantibodies against ACE2 may develop after SARS-CoV-2 infection, as anti-idiotypic antibodies to anti-spike protein antibodies . (bvsalud.org)
  • Autoantibodies make excellent biomarkers in diseases with an inflammatory or autoimmune component. (sengenics.com)
  • 1) defining the different subtypes of autoimmune muscle disease based on muscle histology, autoantibodies, and other biomarkers. (nih.gov)
  • In RA, an increased number of autoantibodies directed against these self-antigens such as rheumatoid factors (RF) and anticitrullinated protein antibody (ACPA) are commonly prevalent. (hindawi.com)
  • Autoantibodies are a type of antibody that attacks healthy cells by mistake. (medlineplus.gov)
  • Incorporation of these additional serological targets increased the sensitivity of autoantibody testing for SS to ~80% without decreasing specificity. (nih.gov)
  • Background: Autoantibodies to zinc transporter 8 (ZnT8A) are usually the last autoantibody specificity to appear in the preclinical phase of type 1 diabetes (T1D). (bris.ac.uk)
  • Rheumatoid arthritis (RA) is one of the most common autoimmune diseases, which affects approximately 1% of the world population, and is characterized by autoantibody production, synovial inflammation, cartilage destruction, and bone erosion [ 1 ]. (hindawi.com)
  • Specificities of anti-neutrophil autoantibodies in patients with rheumatoid arthritis (RA). (ox.ac.uk)
  • Testing of IgG autoantibodies to human cellular antigens was performed by the HEp-2 cell immunofluorescence assay using slides from INOVA Diagnostics, San Diego, CA (Cat # 508100) following the manufacturer's instructions and evaluated primarily using their NOVA View system. (cdc.gov)
  • The objective of this study was to characterize antigens recognized by neutrophil-specific autoantibodies from patients with RA. (ox.ac.uk)
  • In conclusion, anti-neutrophil autoantibodies from RA patients recognize different antigens in the cytoplasm and in the nucleus. (ox.ac.uk)
  • In this review, the diagnostic value of autoantibodies, their synthesis and function as a mediator of joint inflammation, and the significance of IgG-Fc glycosylation are discussed. (hindawi.com)
  • We are currently expanding the autoimmune screening panel to include additional autoantigen targets and are determining the clinical significance of autoantibodies to these targets in individual SS cases. (nih.gov)
  • The remarkable heterogeneity of autoantibodies observed in SS may represent a personalized diagnostic for SS patients and provides insight into the complex nature of this autoimmune disease. (nih.gov)
  • Little is known about the factors that influence autoantibody profiles and the continuation of the autoimmune response post-diagnosis. (bris.ac.uk)
  • Background: Autoimmune chronic spontaneous urticaria (aiCSU) is an important sub‐ type of chronic spontaneous urticaria (CSU) in which functional IgG autoantibodies to IgE or its high‐affinity receptor (FcεRI) induces mast cell degranulation and subsequent symptom. (marcus-maurer.com)
  • Dr. Mammen and his colleagues at Hopkins discovered a novel form of autoimmune myopathy associated with statin use and autoantibodies recognizing HMG-CoA reductase, the pharmacologic target of statins. (nih.gov)
  • Suffice to say these are autoantibodies - where the body mounts an immune response against 'self' - that target a particular protein called folate receptor protein alpha which plays an important role in transporting something called 5-methyltetrahydrofolate (5-MTHF) into the brain. (blogspot.com)
  • A new autoantibody marker called neuromyelitis optica immunoglobulin G (NMO-IgG), which targets the water channel protein aquaporin-4, is highly specific for NMO. (elsevier.com)
  • Questioning Answers: Folate receptor autoantibodies and autism. (blogspot.com)
  • Not only that, they represent scientific replication covering an increasingly important issue in relation to [some] autism: a possible role for folate receptor autoantibodies (FRAA) . (blogspot.com)
  • In short, folate receptor autoantibodies are probably important to at least some autism. (blogspot.com)
  • Folate receptor autoantibodies are prevalent in children diagnosed with autism spectrum disorder, their normal siblings and parents. (blogspot.com)
  • High milk consumers have an increased risk of folate receptor blocking autoantibody production but this does not affect folate status in Spanish men and women. (blogspot.com)
  • Ultimately, the detection of IFN-γ autoantibodies in high levels explained these abnormalities. (cdc.gov)
  • In addition, autoantibodies are proven to be useful disease markers for RA, and different diagnostic tools are being developed for early diagnosis of the clinical disease. (hindawi.com)
  • Background: The anti-DFS70 autoantibodies are one of the most commonly and widely described agent of unknown clinical significance, frequently detected in healthy individuals. (ljmu.ac.uk)
  • Our solutions enable the discovery and validation of autoantibody biomarker signatures for patient stratification, therapeutic response prediction and development of companion diagnostics. (sengenics.com)
  • The interferon- γ (IFN-γ)/interleukin-12 (IL-12) axis is a critical pathway for intracellular killing of mycobacteria ( Technical Appendix Figure) ( 1 ).We report a case of disseminated NTM infection in a woman from Laos who showed IFN-γ autoantibodies. (cdc.gov)
  • Specific treatment for IFN-γ autoantibodies-associated NTM infection is not codified and required prolonged, multiple-drug regimens. (cdc.gov)
  • Development of ACE2 autoantibodies after SARS-CoV-2 infection. (bvsalud.org)
  • 2) elucidating the role of myositis autoantibodies in the pathogenesis of myositis. (nih.gov)
  • Graphs showing difference between normalized RFUs in 8 autoantibodies that were significantly elevated in cases (H. pylori seropositive PD patients, n=30) versus controls (H. pylori sero-negative PD patients, n=30). (sengenics.com)
  • It is not known whether the DFS70 autoantibodies are protective or pathogenic. (ljmu.ac.uk)
  • A large number of studies have found that abnormally increased immune cells (T cells, B cells, macrophages, and neutrophils) and immune molecules (cytokines, autoantibodies, and heat shock proteins) are present in the synovial tissue and fluid of RA patients, which suggest that the release or activation of them may be involved in the initiation and perpetuation of RA. (hindawi.com)
  • Anti-gephyrin autoantibodies have been tied to lower gastrointestinal (GI) dysfunction, such as severe constipation and distention, in patients with systemic sclerosis (SSc), new research suggests. (medscape.com)
  • Afin de comparer la prévalence des autoanticorps positifs chez les patients atteints de troubles thyroïdiens et chez des sujets en bonne santé dans une région riche en iode de la République islamique d'Iran, nous avons effectué une étude clinique sur 930 femmes : 698 patientes (286 hypothyroïdiennes, 140 hyperthyroïdiennes et 272 présentant un goitre simple) et 232 femmes en bonne santé. (who.int)
  • 2016) Augmentation of Autoantibodies by Helicobacter pylori in Parkinson's Disease Patients May Be Linked to Greater Severity. (sengenics.com)
  • The autoantibodies were titrated by ELISA in 202 samples of pemphigus foliaceus, 131 pemphigus vulgaris, 50 and 57 relatives of patients with pemphigus foliaceus and pemphigus vulgaris, respectively, and 114 controls. (anaisdedermatologia.org.br)
  • The phenotype of myositis patients with anti-Ku autoantibodies. (nih.gov)
  • Among those elevated were autoantibodies that recognize Nuclear factor I subtype A (NFIA), Platelet-derived growth factor B (PDGFB) and Eukaryotic translation initiation factor 4A3 (eIFA3) - all proteins involved in normal neurological function. (sengenics.com)
  • Recently several novel autoantibodies against a variety of specific nuclear pore proteins have been described, including the nucleoporin p62. (openrheumatologyjournal.com)
  • The determination of autoantibody titers from 1:80 to 1:1280 was performed by serial dilution on samples that showed a 3+ or greater nuclear and/or cytoplasmic immunofluorescence pattern. (cdc.gov)
  • Various genetic and environmental factors are associated with autoantibody production against different autoantigenic targets. (hindawi.com)
  • Only C3 NeF type II were found to be associated with circulating autoantibodies to the collagenous region of C1q (aC1qCLR). (avhandlingar.se)
  • A significant association was found between RM, and autoantibodies in the 'aTG + aTPO + anti-ENA' or 'aTG + aTPO' panels. (biu.ac.il)
  • Autoantibodies were found. (medlineplus.gov)
  • She tested negative for hepatitis markers and for autoantibodies. (nih.gov)
  • I and II) Autoantibodies to the C3 cleaving enzyme complex of the alternative pathway, C3 nephritic factors (C3 NeF), cause partial C3 deficiency and are associated with increased susceptibility to bacterial infections. (avhandlingar.se)
  • Reduction in White Blood Cell, Neutrophil, and Red Blood Cell Counts Related to Sex, HLA, and Islet Autoantibodies in Swedish TEDDY Children at Increased Risk for Type 1 Diabetes. (arctichealth.org)
  • AVHANDLINGAR.SE: Complement aberrations and autoantibodies to complement proteins in relation to disease mechanisms. (avhandlingar.se)
  • This acquired autoantibodies-mediated immunodeficiency is more frequent among women, in whom the disease typically manifests in the second half of adult life (median 48 [IQR 44.8-60.0] years of age). (cdc.gov)
  • Anti-mitochondrial autoantibodies are associated with cardiomyopathy, dysphagia, and features of more severe disease in adult-onset myositis. (nih.gov)
  • Conclusions: RM was associated with autoantibodies to aTPO and the combined panel of aTPO, aTG and anti-ENA, but not with aPL. (biu.ac.il)
  • IFN-γ autoantibodies remained positive at the time of this report, 2 years after azithromycin initiation. (cdc.gov)
  • That patient had GI dysfunction but no defined SSc-associated autoantibodies. (medscape.com)