A molecule that binds to another molecule, used especially to refer to a small molecule that binds specifically to a larger molecule, e.g., an antigen binding to an antibody, a hormone or neurotransmitter binding to a receptor, or a substrate or allosteric effector binding to an enzyme. Ligands are also molecules that donate or accept a pair of electrons to form a coordinate covalent bond with the central metal atom of a coordination complex. (From Dorland, 27th ed)
A membrane glycoprotein and differentiation antigen expressed on the surface of T-cells that binds to CD40 ANTIGENS on B-LYMPHOCYTES and induces their proliferation. Mutation of the gene for CD40 ligand is a cause of HYPER-IGM IMMUNODEFICIENCY SYNDROME, TYPE 1.
Differentiation antigens found on thymocytes and on cytotoxic and suppressor T-lymphocytes. CD8 antigens are members of the immunoglobulin supergene family and are associative recognition elements in MHC (Major Histocompatibility Complex) Class I-restricted interactions.
Complex of at least five membrane-bound polypeptides in mature T-lymphocytes that are non-covalently associated with one another and with the T-cell receptor (RECEPTORS, ANTIGEN, T-CELL). The CD3 complex includes the gamma, delta, epsilon, zeta, and eta chains (subunits). When antigen binds to the T-cell receptor, the CD3 complex transduces the activating signals to the cytoplasm of the T-cell. The CD3 gamma and delta chains (subunits) are separate from and not related to the gamma/delta chains of the T-cell receptor (RECEPTORS, ANTIGEN, T-CELL, GAMMA-DELTA).
A member of the tumor necrosis factor receptor superfamily with specificity for CD40 LIGAND. It is found on mature B-LYMPHOCYTES and some EPITHELIAL CELLS, lymphoid DENDRITIC CELLS. Evidence suggests that CD40-dependent activation of B-cells is important for generation of memory B-cells within the germinal centers. Mutations of the gene for CD40 antigen result in HYPER-IGM IMMUNODEFICIENCY SYNDROME, TYPE 3. Signaling of the receptor occurs through its association with TNF RECEPTOR-ASSOCIATED FACTORS.
Acidic sulfated integral membrane glycoproteins expressed in several alternatively spliced and variable glycosylated forms on a wide variety of cell types including mature T-cells, B-cells, medullary thymocytes, granulocytes, macrophages, erythrocytes, and fibroblasts. CD44 antigens are the principle cell surface receptors for hyaluronate and this interaction mediates binding of lymphocytes to high endothelial venules. (From Abbas et al., Cellular and Molecular Immunology, 2d ed, p156)
Glycoproteins found on immature hematopoietic cells and endothelial cells. They are the only molecules to date whose expression within the blood system is restricted to a small number of progenitor cells in the bone marrow.
Costimulatory T-LYMPHOCYTE receptors that have specificity for CD80 ANTIGEN and CD86 ANTIGEN. Activation of this receptor results in increased T-cell proliferation, cytokine production and promotion of T-cell survival.
Ratio of T-LYMPHOCYTES that express the CD4 ANTIGEN to those that express the CD8 ANTIGEN. This value is commonly assessed in the diagnosis and staging of diseases affecting the IMMUNE SYSTEM including HIV INFECTIONS.
Glycolipid-anchored membrane glycoproteins expressed on cells of the myelomonocyte lineage including monocytes, macrophages, and some granulocytes. They function as receptors for the complex of lipopolysaccharide (LPS) and LPS-binding protein.
A bifunctional enzyme that catalyzes the synthesis and HYDROLYSIS of CYCLIC ADP-RIBOSE (cADPR) from NAD+ to ADP-RIBOSE. It is a cell surface molecule which is predominantly expressed on LYMPHOID CELLS and MYELOID CELLS.
A critical subpopulation of T-lymphocytes involved in the induction of most immunological functions. The HIV virus has selective tropism for the T4 cell which expresses the CD4 phenotypic marker, a receptor for HIV. In fact, the key element in the profound immunosuppression seen in HIV infection is the depletion of this subset of T-lymphocytes.
A costimulatory ligand expressed by ANTIGEN-PRESENTING CELLS that binds to CTLA-4 ANTIGEN with high specificity and to CD28 ANTIGEN with low specificity. The interaction of CD80 with CD28 ANTIGEN provides a costimulatory signal to T-LYMPHOCYTES, while its interaction with CTLA-4 ANTIGEN may play a role in inducing PERIPHERAL TOLERANCE.
Glycoproteins expressed on cortical thymocytes and on some dendritic cells and B-cells. Their structure is similar to that of MHC Class I and their function has been postulated as similar also. CD1 antigens are highly specific markers for human LANGERHANS CELLS.
A tumor necrosis factor receptor subtype found in a variety of tissues and on activated LYMPHOCYTES. It has specificity for FAS LIGAND and plays a role in regulation of peripheral immune responses and APOPTOSIS. Multiple isoforms of the protein exist due to multiple ALTERNATIVE SPLICING. The activated receptor signals via a conserved death domain that associates with specific TNF RECEPTOR-ASSOCIATED FACTORS in the CYTOPLASM.
Differentiation antigens residing on mammalian leukocytes. CD stands for cluster of differentiation, which refers to groups of monoclonal antibodies that show similar reactivity with certain subpopulations of antigens of a particular lineage or differentiation stage. The subpopulations of antigens are also known by the same CD designation.
Glycoprotein members of the immunoglobulin superfamily which participate in T-cell adhesion and activation. They are expressed on most peripheral T-lymphocytes, natural killer cells, and thymocytes, and function as co-receptors or accessory molecules in the T-cell receptor complex.
A costimulatory ligand expressed by ANTIGEN-PRESENTING CELLS that binds to CD28 ANTIGEN with high specificity and to CTLA-4 ANTIGEN with low specificity. The interaction of CD86 with CD28 ANTIGEN provides a stimulatory signal to T-LYMPHOCYTES, while its interaction with CTLA-4 ANTIGEN may play a role in inducing PERIPHERAL TOLERANCE.
Differentiation antigens expressed on B-lymphocytes and B-cell precursors. They are involved in regulation of B-cell proliferation.
Glycoproteins expressed on all mature T-cells, thymocytes, and a subset of mature B-cells. Antibodies specific for CD5 can enhance T-cell receptor-mediated T-cell activation. The B-cell-specific molecule CD72 is a natural ligand for CD5. (From Abbas et al., Cellular and Molecular Immunology, 2d ed, p156)
Cell-surface glycoprotein beta-chains that are non-covalently linked to specific alpha-chains of the CD11 family of leukocyte-adhesion molecules (RECEPTORS, LEUKOCYTE-ADHESION). A defect in the gene encoding CD18 causes LEUKOCYTE-ADHESION DEFICIENCY SYNDROME.
A transmembrane protein belonging to the tumor necrosis factor superfamily that was originally discovered on cells of the lymphoid-myeloid lineage, including activated T-LYMPHOCYTES and NATURAL KILLER CELLS. It plays an important role in immune homeostasis and cell-mediated toxicity by binding to the FAS RECEPTOR and triggering APOPTOSIS.
The 140 kDa isoform of NCAM (neural cell adhesion molecule) containing a transmembrane domain and short cytoplasmic tail. It is expressed by all lymphocytes mediating non-MHC restricted cytotoxicity and is present on some neural tissues and tumors.
A membrane-bound tumor necrosis family member found primarily on activated T-LYMPHOCYTES that binds specifically to CD30 ANTIGEN. It may play a role in INFLAMMATION and immune regulation.
A member of the tumor necrosis factor receptor superfamily that may play a role in the regulation of NF-KAPPA B and APOPTOSIS. They are found on activated T-LYMPHOCYTES; B-LYMPHOCYTES; NEUTROPHILS; EOSINOPHILS; MAST CELLS and NK CELLS. Overexpression of CD30 antigen in hematopoietic malignancies make the antigen clinically useful as a biological tumor marker. Signaling of the receptor occurs through its association with TNF RECEPTOR-ASSOCIATED FACTORS.
Leukocyte differentiation antigens and major platelet membrane glycoproteins present on MONOCYTES; ENDOTHELIAL CELLS; PLATELETS; and mammary EPITHELIAL CELLS. They play major roles in CELL ADHESION; SIGNAL TRANSDUCTION; and regulation of angiogenesis. CD36 is a receptor for THROMBOSPONDINS and can act as a scavenger receptor that recognizes and transports oxidized LIPOPROTEINS and FATTY ACIDS.
A cell adhesion protein that was originally identified as a heat stable antigen in mice. It is involved in METASTASIS and is highly expressed in many NEOPLASMS.
A subtype of tetraspanin proteins that play a role in cell adhesion, cell motility, and tumor metastasis. CD9 antigens take part in the process of platelet activation and aggregation, the formation of paranodal junctions in neuronal tissue, and the fusion of sperm with egg.
A critical subpopulation of regulatory T-lymphocytes involved in MHC Class I-restricted interactions. They include both cytotoxic T-lymphocytes (T-LYMPHOCYTES, CYTOTOXIC) and CD8+ suppressor T-lymphocytes.
A sialic acid-rich protein and an integral cell membrane mucin. It plays an important role in activation of T-LYMPHOCYTES.
Differentiation antigens expressed on pluripotential hematopoietic cells, most human thymocytes, and a major subset of peripheral blood T-lymphocytes. They have been implicated in integrin-mediated cellular adhesion and as signalling receptors on T-cells.
Unglycosylated phosphoproteins expressed only on B-cells. They are regulators of transmembrane Ca2+ conductance and thought to play a role in B-cell activation and proliferation.
A group of three different alpha chains (CD11a, CD11b, CD11c) that are associated with an invariant CD18 beta chain (ANTIGENS, CD18). The three resulting leukocyte-adhesion molecules (RECEPTORS, LEUKOCYTE ADHESION) are LYMPHOCYTE FUNCTION-ASSOCIATED ANTIGEN-1; MACROPHAGE-1 ANTIGEN; and ANTIGEN, P150,95.
A transmembrane protein belonging to the tumor necrosis factor superfamily that specifically binds to CD27 ANTIGEN. It is found on activated T-LYMPHOCYTES; B-LYMPHOCYTES; and DENDRITIC CELLS where it plays a role in stimulating the proliferation of CD4-POSITIVE T-LYMPHOCYTES and CD8-POSITIVE T-LYMPHOCYTES.
A ubiquitously expressed membrane glycoprotein. It interacts with a variety of INTEGRINS and mediates responses to EXTRACELLULAR MATRIX PROTEINS.
Small glycoproteins found on both hematopoietic and non-hematopoietic cells. CD59 restricts the cytolytic activity of homologous complement by binding to C8 and C9 and blocking the assembly of the membrane attack complex. (From Barclay et al., The Leukocyte Antigen FactsBook, 1993, p234)
A CD antigen that contains a conserved I domain which is involved in ligand binding. When combined with CD18 the two subunits form MACROPHAGE-1 ANTIGEN.
A ubiquitously expressed complement receptor that binds COMPLEMENT C3B and COMPLEMENT C4B and serves as a cofactor for their inactivation. CD46 also interacts with a wide variety of pathogens and mediates immune response.
The number of CD4-POSITIVE T-LYMPHOCYTES per unit volume of BLOOD. Determination requires the use of a fluorescence-activated flow cytometer.
Oligosaccharide antigenic determinants found principally on NK cells and T-cells. Their role in the immune response is poorly understood.
The process in which substances, either endogenous or exogenous, bind to proteins, peptides, enzymes, protein precursors, or allied compounds. Specific protein-binding measures are often used as assays in diagnostic assessments.
Tetraspanin proteins that are involved in a variety of cellular functions including BASEMENT MEMBRANE assembly, and in the formation of a molecular complexes on the surface of LYMPHOCYTES.
A member of the tumor necrosis factor receptor superfamily that is specific for 4-1BB LIGAND. It is found in a variety of immune cell types including activated T-LYMPHOCYTES; NATURAL KILLER CELLS; and DENDRITIC CELLS. Activation of the receptor on T-LYMPHOCYTES plays a role in their expansion, production of cytokines and survival. Signaling by the activated receptor occurs through its association with TNF RECEPTOR-ASSOCIATED FACTORS.
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.
An integrin alpha subunit of approximately 150-kDa molecular weight. It is expressed at high levels on monocytes and combines with CD18 ANTIGEN to form the cell surface receptor INTEGRIN ALPHAXBETA2. The subunit contains a conserved I-domain which is characteristic of several of alpha integrins.
Cell adhesion molecules present on virtually all monocytes, platelets, and granulocytes. CD31 is highly expressed on endothelial cells and concentrated at the junctions between them.
Glycoproteins with a wide distribution on hematopoietic and non-hematopoietic cells and strongly expressed on macrophages. CD58 mediates cell adhesion by binding to CD2; (ANTIGENS, CD2); and this enhances antigen-specific T-cell activation.
GPI-linked membrane proteins broadly distributed among hematopoietic and non-hematopoietic cells. CD55 prevents the assembly of C3 CONVERTASE or accelerates the disassembly of preformed convertase, thus blocking the formation of the membrane attack complex.
Tetraspanin proteins found associated with LAMININ-binding INTEGRINS. The CD151 antigens may play a role in the regulation of CELL MOTILITY.
The parts of a macromolecule that directly participate in its specific combination with another molecule.
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.
A transmembrane protein belonging to the tumor necrosis factor superfamily that specifically binds RECEPTOR ACTIVATOR OF NUCLEAR FACTOR-KAPPA B and OSTEOPROTEGERIN. It plays an important role in regulating OSTEOCLAST differentiation and activation.
Ubiquitously-expressed tetraspanin proteins that are found in late ENDOSOMES and LYSOSOMES and have been implicated in intracellular transport of proteins.
Zinc-binding metalloproteases that are members of the type II integral membrane metalloproteases. They are expressed by GRANULOCYTES; MONOCYTES; and their precursors as well as by various non-hematopoietic cells. They release an N-terminal amino acid from a peptide, amide or arylamide.
An alpha-integrin subunit found on lymphocytes, granulocytes, macrophages and monocytes. It combines with the integrin beta2 subunit (CD18 ANTIGEN) to form LYMPHOCYTE FUNCTION-ASSOCIATED ANTIGEN-1.
Glycoproteins found on the membrane or surface of cells.
Established cell cultures that have the potential to propagate indefinitely.
Models used experimentally or theoretically to study molecular shape, electronic properties, or interactions; includes analogous molecules, computer-generated graphics, and mechanical structures.
Process of classifying cells of the immune system based on structural and functional differences. The process is commonly used to analyze and sort T-lymphocytes into subsets based on CD antigens by the technique of flow cytometry.
Technique using an instrument system for making, processing, and displaying one or more measurements on individual cells obtained from a cell suspension. Cells are usually stained with one or more fluorescent dyes specific to cell components of interest, e.g., DNA, and fluorescence of each cell is measured as it rapidly transverses the excitation beam (laser or mercury arc lamp). Fluorescence provides a quantitative measure of various biochemical and biophysical properties of the cell, as well as a basis for cell sorting. Other measurable optical parameters include light absorption and light scattering, the latter being applicable to the measurement of cell size, shape, density, granularity, and stain uptake.
The intracellular transfer of information (biological activation/inhibition) through a signal pathway. In each signal transduction system, an activation/inhibition signal from a biologically active molecule (hormone, neurotransmitter) is mediated via the coupling of a receptor/enzyme to a second messenger system or to an ion channel. Signal transduction plays an important role in activating cellular functions, cell differentiation, and cell proliferation. Examples of signal transduction systems are the GAMMA-AMINOBUTYRIC ACID-postsynaptic receptor-calcium ion channel system, the receptor-mediated T-cell activation pathway, and the receptor-mediated activation of phospholipases. Those coupled to membrane depolarization or intracellular release of calcium include the receptor-mediated activation of cytotoxic functions in granulocytes and the synaptic potentiation of protein kinase activation. Some signal transduction pathways may be part of larger signal transduction pathways; for example, protein kinase activation is part of the platelet activation signal pathway.
An inhibitory B7 antigen that has specificity for the T-CELL receptor PROGRAMMED CELL DEATH 1 PROTEIN. CD274 antigen provides negative signals that control and inhibit T-cell responses and is found at higher than normal levels on tumor cells, suggesting its potential role in TUMOR IMMUNE EVASION.
A widely distributed cell surface transmembrane glycoprotein that stimulates the synthesis of MATRIX METALLOPROTEINASES. It is found at high levels on the surface of malignant NEOPLASMS and may play a role as a mediator of malignant cell behavior.
Specialized cells of the hematopoietic system that have branch-like extensions. They are found throughout the lymphatic system, and in non-lymphoid tissues such as SKIN and the epithelia of the intestinal, respiratory, and reproductive tracts. They trap and process ANTIGENS, and present them to T-CELLS, thereby stimulating CELL-MEDIATED IMMUNITY. They are different from the non-hematopoietic FOLLICULAR DENDRITIC CELLS, which have a similar morphology and immune system function, but with respect to humoral immunity (ANTIBODY PRODUCTION).
A widely expressed transmembrane glycoprotein that functions as a METASTASIS suppressor protein. It is underexpressed in a variety of human NEOPLASMS.
A transmembrane-protein belonging to the TNF family of intercellular signaling proteins. It is a widely expressed ligand that activates APOPTOSIS by binding to TNF-RELATED APOPTOSIS-INDUCING LIGAND RECEPTORS. The membrane-bound form of the protein can be cleaved by specific CYSTEINE ENDOPEPTIDASES to form a soluble ligand form.
Laboratory mice that have been produced from a genetically manipulated EGG or EMBRYO, MAMMALIAN.
Molecules on the surface of T-lymphocytes that recognize and combine with antigens. The receptors are non-covalently associated with a complex of several polypeptides collectively called CD3 antigens (ANTIGENS, CD3). Recognition of foreign antigen and the major histocompatibility complex is accomplished by a single heterodimeric antigen-receptor structure, composed of either alpha-beta (RECEPTORS, ANTIGEN, T-CELL, ALPHA-BETA) or gamma-delta (RECEPTORS, ANTIGEN, T-CELL, GAMMA-DELTA) chains.
Non-antibody proteins secreted by inflammatory leukocytes and some non-leukocytic cells, that act as intercellular mediators. They differ from classical hormones in that they are produced by a number of tissue or cell types rather than by specialized glands. They generally act locally in a paracrine or autocrine rather than endocrine manner.
The rate dynamics in chemical or physical systems.
Cell surface proteins that bind signalling molecules external to the cell with high affinity and convert this extracellular event into one or more intracellular signals that alter the behavior of the target cell (From Alberts, Molecular Biology of the Cell, 2nd ed, pp693-5). Cell surface receptors, unlike enzymes, do not chemically alter their ligands.
The level of protein structure in which combinations of secondary protein structures (alpha helices, beta sheets, loop regions, and motifs) pack together to form folded shapes called domains. Disulfide bridges between cysteines in two different parts of the polypeptide chain along with other interactions between the chains play a role in the formation and stabilization of tertiary structure. Small proteins usually consist of only one domain but larger proteins may contain a number of domains connected by segments of polypeptide chain which lack regular secondary structure.
Cells propagated in vitro in special media conducive to their growth. Cultured cells are used to study developmental, morphologic, metabolic, physiologic, and genetic processes, among others.
Proteins prepared by recombinant DNA technology.
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.
Proteins which are found in membranes including cellular and intracellular membranes. They consist of two types, peripheral and integral proteins. They include most membrane-associated enzymes, antigenic proteins, transport proteins, and drug, hormone, and lectin receptors.
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.
Antigens expressed on the cell membrane of T-lymphocytes during differentiation, activation, and normal and neoplastic transformation. Their phenotypic characterization is important in differential diagnosis and studies of thymic ontogeny and T-cell function.
Cell surface molecules on cells of the immune system that specifically bind surface molecules or messenger molecules and trigger changes in the behavior of cells. Although these receptors were first identified in the immune system, many have important functions elsewhere.
The altered state of immunologic responsiveness resulting from initial contact with antigen, which enables the individual to produce antibodies more rapidly and in greater quantity in response to secondary antigenic stimulus.
One of the mechanisms by which CELL DEATH occurs (compare with NECROSIS and AUTOPHAGOCYTOSIS). Apoptosis is the mechanism responsible for the physiological deletion of cells and appears to be intrinsically programmed. It is characterized by distinctive morphologic changes in the nucleus and cytoplasm, chromatin cleavage at regularly spaced sites, and the endonucleolytic cleavage of genomic DNA; (DNA FRAGMENTATION); at internucleosomal sites. This mode of cell death serves as a balance to mitosis in regulating the size of animal tissues and in mediating pathologic processes associated with tumor growth.
A cell adhesion molecule of the immunoglobulin superfamily that is expressed in ENDOTHELIAL CELLS and is involved in INTERCELLULAR JUNCTIONS.
The characteristic 3-dimensional shape of a protein, including the secondary, supersecondary (motifs), tertiary (domains) and quaternary structure of the peptide chain. PROTEIN STRUCTURE, QUATERNARY describes the conformation assumed by multimeric proteins (aggregates of more than one polypeptide chain).
A trisaccharide antigen expressed on glycolipids and many cell-surface glycoproteins. In the blood the antigen is found on the surface of NEUTROPHILS; EOSINOPHILS; and MONOCYTES. In addition, CD15 antigen is a stage-specific embryonic antigen.
Antigens expressed primarily on the membranes of living cells during sequential stages of maturation and differentiation. As immunologic markers they have high organ and tissue specificity and are useful as probes in studies of normal cell development as well as neoplastic transformation.
Members of the class of compounds composed of AMINO ACIDS joined together by peptide bonds between adjacent amino acids into linear, branched or cyclical structures. OLIGOPEPTIDES are composed of approximately 2-12 amino acids. Polypeptides are composed of approximately 13 or more amino acids. PROTEINS are linear polypeptides that are normally synthesized on RIBOSOMES.
A membrane bound member of the TNF superfamily that is expressed on activated B-LYMPHOCYTES; MACROPHAGES; and DENDRITIC CELLS. The ligand is specific for the 4-1BB RECEPTOR and may play a role in inducing the proliferation of activated peripheral blood T-LYMPHOCYTES.
RNA sequences that serve as templates for protein synthesis. Bacterial mRNAs are generally primary transcripts in that they do not require post-transcriptional processing. Eukaryotic mRNA is synthesized in the nucleus and must be exported to the cytoplasm for translation. Most eukaryotic mRNAs have a sequence of polyadenylic acid at the 3' end, referred to as the poly(A) tail. The function of this tail is not known for certain, but it may play a role in the export of mature mRNA from the nucleus as well as in helping stabilize some mRNA molecules by retarding their degradation in the cytoplasm.
A membrane-bound tumor necrosis family member that is expressed on activated antigen-presenting cells such as B-LYMPHOCYTES and MACROPHAGES. It signals T-LYMPHOCYTES by binding the OX40 RECEPTOR.
Bone marrow-derived lymphocytes that possess cytotoxic properties, classically directed against transformed and virus-infected cells. Unlike T CELLS; and B CELLS; NK CELLS are not antigen specific. The cytotoxicity of natural killer cells is determined by the collective signaling of an array of inhibitory and stimulatory CELL SURFACE RECEPTORS. A subset of T-LYMPHOCYTES referred to as NATURAL KILLER T CELLS shares some of the properties of this cell type.
The uptake of naked or purified DNA by CELLS, usually meaning the process as it occurs in eukaryotic cells. It is analogous to bacterial transformation (TRANSFORMATION, BACTERIAL) and both are routinely employed in GENE TRANSFER TECHNIQUES.
CD4-positive T cells that inhibit immunopathology or autoimmune disease in vivo. They inhibit the immune response by influencing the activity of other cell types. Regulatory T-cells include naturally occurring CD4+CD25+ cells, IL-10 secreting Tr1 cells, and Th3 cells.
Adherence of cells to surfaces or to other cells.
Morphologic alteration of small B LYMPHOCYTES or T LYMPHOCYTES in culture into large blast-like cells able to synthesize DNA and RNA and to divide mitotically. It is induced by INTERLEUKINS; MITOGENS such as PHYTOHEMAGGLUTININS, and by specific ANTIGENS. It may also occur in vivo as in GRAFT REJECTION.
All of the processes involved in increasing CELL NUMBER including CELL DIVISION.
The sequence of PURINES and PYRIMIDINES in nucleic acids and polynucleotides. It is also called nucleotide sequence.
The interaction of two or more substrates or ligands with the same binding site. The displacement of one by the other is used in quantitative and selective affinity measurements.
Recombinant proteins produced by the GENETIC TRANSLATION of fused genes formed by the combination of NUCLEIC ACID REGULATORY SEQUENCES of one or more genes with the protein coding sequences of one or more genes.
A single, unpaired primary lymphoid organ situated in the MEDIASTINUM, extending superiorly into the neck to the lower edge of the THYROID GLAND and inferiorly to the fourth costal cartilage. It is necessary for normal development of immunologic function early in life. By puberty, it begins to involute and much of the tissue is replaced by fat.
Integrin beta-1 chains which are expressed as heterodimers that are noncovalently associated with specific alpha-chains of the CD49 family (CD49a-f). CD29 is expressed on resting and activated leukocytes and is a marker for all of the very late activation antigens on cells. (from: Barclay et al., The Leukocyte Antigen FactsBook, 1993, p164)
A cell line derived from cultured tumor cells.
A soluble substance elaborated by antigen- or mitogen-stimulated T-LYMPHOCYTES which induces DNA synthesis in naive lymphocytes.
The phenomenon of target cell destruction by immunologically active effector cells. It may be brought about directly by sensitized T-lymphocytes or by lymphoid or myeloid "killer" cells, or it may be mediated by cytotoxic antibody, cytotoxic factor released by lymphoid cells, or complement.
The study of crystal structure using X-RAY DIFFRACTION techniques. (McGraw-Hill Dictionary of Scientific and Technical Terms, 4th ed)
Any of the processes by which nuclear, cytoplasmic, or intercellular factors influence the differential control (induction or repression) of gene action at the level of transcription or translation.
A component of the B-cell antigen receptor that is involved in B-cell antigen receptor heavy chain transport to the PLASMA MEMBRANE. It is expressed almost exclusively in B-LYMPHOCYTES and serves as a useful marker for B-cell NEOPLASMS.
An encapsulated lymphatic organ through which venous blood filters.
CELL LINE derived from the ovary of the Chinese hamster, Cricetulus griseus (CRICETULUS). The species is a favorite for cytogenetic studies because of its small chromosome number. The cell line has provided model systems for the study of genetic alterations in cultured mammalian cells.
A positive regulatory effect on physiological processes at the molecular, cellular, or systemic level. At the molecular level, the major regulatory sites include membrane receptors, genes (GENE EXPRESSION REGULATION), mRNAs (RNA, MESSENGER), and proteins.
Cells grown in vitro from neoplastic tissue. If they can be established as a TUMOR CELL LINE, they can be propagated in cell culture indefinitely.
A heterodimeric protein that is a cell surface antigen associated with lymphocyte activation. The initial characterization of this protein revealed one identifiable heavy chain (ANTIGENS, CD98 HEAVY CHAIN) and an indeterminate smaller light chain. It is now known that a variety of light chain subunits (ANTIGENS, CD98 LIGHT CHAINS) can dimerize with the heavy chain. Depending upon its light chain composition a diverse array of functions can be found for this protein. Functions include: type L amino acid transport, type y+L amino acid transport and regulation of cellular fusion.
The relationship between the chemical structure of a compound and its biological or pharmacological activity. Compounds are often classed together because they have structural characteristics in common including shape, size, stereochemical arrangement, and distribution of functional groups.
Strains of mice in which certain GENES of their GENOMES have been disrupted, or "knocked-out". To produce knockouts, using RECOMBINANT DNA technology, the normal DNA sequence of the gene being studied is altered to prevent synthesis of a normal gene product. Cloned cells in which this DNA alteration is successful are then injected into mouse EMBRYOS to produce chimeric mice. The chimeric mice are then bred to yield a strain in which all the cells of the mouse contain the disrupted gene. Knockout mice are used as EXPERIMENTAL ANIMAL MODELS for diseases (DISEASE MODELS, ANIMAL) and to clarify the functions of the genes.
A class of animal lectins that bind to carbohydrate in a calcium-dependent manner. They share a common carbohydrate-binding domain that is structurally distinct from other classes of lectins.
The movement of cells from one location to another. Distinguish from CYTOKINESIS which is the process of dividing the CYTOPLASM of a cell.
Large, phagocytic mononuclear leukocytes produced in the vertebrate BONE MARROW and released into the BLOOD; contain a large, oval or somewhat indented nucleus surrounded by voluminous cytoplasm and numerous organelles.
A sialomucin protein that functions as a cell adhesion molecule. It is a negative regulator of certain types of HEMATOPOIETIC STEM CELLS.
A variation of the PCR technique in which cDNA is made from RNA via reverse transcription. The resultant cDNA is then amplified using standard PCR protocols.
A technique of culturing mixed cell types in vitro to allow their synergistic or antagonistic interactions, such as on CELL DIFFERENTIATION or APOPTOSIS. Coculture can be of different types of cells, tissues, or organs from normal or disease states.
Transport proteins that carry specific substances in the blood or across cell membranes.
A low affinity interleukin-2 receptor subunit that combines with the INTERLEUKIN-2 RECEPTOR BETA SUBUNIT and the INTERLEUKIN RECEPTOR COMMON GAMMA-CHAIN to form a high affinity receptor for INTERLEUKIN-2.
A subfamily in the family MURIDAE, comprising the hamsters. Four of the more common genera are Cricetus, CRICETULUS; MESOCRICETUS; and PHODOPUS.
Progenitor cells from which all blood cells derive.
Antigenic determinants recognized and bound by the T-cell receptor. Epitopes recognized by the T-cell receptor are often located in the inner, unexposed side of the antigen, and become accessible to the T-cell receptors after proteolytic processing of the antigen.
Tetraspanin proteins found at high levels in cells of the lymphoid-myeloid lineage. CD53 antigens may be involved regulating the differentiation of T-LYMPHOCYTES and the activation of B-LYMPHOCYTES.
The number of LYMPHOCYTES per unit volume of BLOOD.
The location of the atoms, groups or ions relative to one another in a molecule, as well as the number, type and location of covalent bonds.
Cell adhesion molecule and CD antigen that serves as a homing receptor for lymphocytes to lymph node high endothelial venules.
Progressive restriction of the developmental potential and increasing specialization of function that leads to the formation of specialized cells, tissues, and organs.
Serum glycoprotein produced by activated MACROPHAGES and other mammalian MONONUCLEAR LEUKOCYTES. It has necrotizing activity against tumor cell lines and increases ability to reject tumor transplants. Also known as TNF-alpha, it is only 30% homologous to TNF-beta (LYMPHOTOXIN), but they share TNF RECEPTORS.
A CELL LINE derived from human T-CELL LEUKEMIA and used to determine the mechanism of differential susceptibility to anti-cancer drugs and radiation.
A negative regulatory effect on physiological processes at the molecular, cellular, or systemic level. At the molecular level, the major regulatory sites include membrane receptors, genes (GENE EXPRESSION REGULATION), mRNAs (RNA, MESSENGER), and proteins.
A costimulatory B7 antigen that has specificity for the T-CELL receptor PROGRAMMED CELL DEATH 1 RECEPTOR. It is closely-related to CD274 antigen; however, its expression is restricted to DENDRITIC CELLS and activated MACROPHAGES.
Partial proteins formed by partial hydrolysis of complete proteins or generated through PROTEIN ENGINEERING techniques.
The type species of LENTIVIRUS and the etiologic agent of AIDS. It is characterized by its cytopathic effect and affinity for the T4-lymphocyte.
Antibodies produced by a single clone of cells.
The lipid- and protein-containing, selectively permeable membrane that surrounds the cytoplasm in prokaryotic and eukaryotic cells.
Form of passive immunization where previously sensitized immunologic agents (cells or serum) are transferred to non-immune recipients. When transfer of cells is used as a therapy for the treatment of neoplasms, it is called adoptive immunotherapy (IMMUNOTHERAPY, ADOPTIVE).
Histochemical localization of immunoreactive substances using labeled antibodies as reagents.
Immunized T-lymphocytes which can directly destroy appropriate target cells. These cytotoxic lymphocytes may be generated in vitro in mixed lymphocyte cultures (MLC), in vivo during a graft-versus-host (GVH) reaction, or after immunization with an allograft, tumor cell or virally transformed or chemically modified target cell. The lytic phenomenon is sometimes referred to as cell-mediated lympholysis (CML). These CD8-positive cells are distinct from NATURAL KILLER CELLS and NATURAL KILLER T-CELLS. There are two effector phenotypes: TC1 and TC2.
Receptors present on activated T-LYMPHOCYTES and B-LYMPHOCYTES that are specific for INTERLEUKIN-2 and play an important role in LYMPHOCYTE ACTIVATION. They are heterotrimeric proteins consisting of the INTERLEUKIN-2 RECEPTOR ALPHA SUBUNIT, the INTERLEUKIN-2 RECEPTOR BETA SUBUNIT, and the INTERLEUKIN RECEPTOR COMMON GAMMA-CHAIN.
Elements of limited time intervals, contributing to particular results or situations.
The fission of a CELL. It includes CYTOKINESIS, when the CYTOPLASM of a cell is divided, and CELL NUCLEUS DIVISION.
The phenotypic manifestation of a gene or genes by the processes of GENETIC TRANSCRIPTION and GENETIC TRANSLATION.
Any detectable and heritable change in the genetic material that causes a change in the GENOTYPE and which is transmitted to daughter cells and to succeeding generations.
T-cell receptors composed of CD3-associated alpha and beta polypeptide chains and expressed primarily in CD4+ or CD8+ T-cells. Unlike immunoglobulins, the alpha-beta T-cell receptors recognize antigens only when presented in association with major histocompatibility (MHC) molecules.
The relatively long-lived phagocytic cell of mammalian tissues that are derived from blood MONOCYTES. Main types are PERITONEAL MACROPHAGES; ALVEOLAR MACROPHAGES; HISTIOCYTES; KUPFFER CELLS of the liver; and OSTEOCLASTS. They may further differentiate within chronic inflammatory lesions to EPITHELIOID CELLS or may fuse to form FOREIGN BODY GIANT CELLS or LANGHANS GIANT CELLS. (from The Dictionary of Cell Biology, Lackie and Dow, 3rd ed.)
Conjugated protein-carbohydrate compounds including mucins, mucoid, and amyloid glycoproteins.
Surface antigens expressed on myeloid cells of the granulocyte-monocyte-histiocyte series during differentiation. Analysis of their reactivity in normal and malignant myelomonocytic cells is useful in identifying and classifying human leukemias and lymphomas.
A heterogeneous group of immunocompetent cells that mediate the cellular immune response by processing and presenting antigens to the T-cells. Traditional antigen-presenting cells include MACROPHAGES; DENDRITIC CELLS; LANGERHANS CELLS; and B-LYMPHOCYTES. FOLLICULAR DENDRITIC CELLS are not traditional antigen-presenting cells, but because they hold antigen on their cell surface in the form of IMMUNE COMPLEXES for B-cell recognition they are considered so by some authors.
Genetically engineered MUTAGENESIS at a specific site in the DNA molecule that introduces a base substitution, or an insertion or deletion.
The outward appearance of the individual. It is the product of interactions between genes, and between the GENOTYPE and the environment.
Cell surface receptors that bind TUMOR NECROSIS FACTORS and trigger changes which influence the behavior of cells.
Tumor necrosis factor receptor family members that are widely expressed and play a role in regulation of peripheral immune responses and APOPTOSIS. The receptors are specific for TNF-RELATED APOPTOSIS-INDUCING LIGAND and signal via conserved death domains that associate with specific TNF RECEPTOR-ASSOCIATED FACTORS in the CYTOPLASM.
A subclass of winged helix DNA-binding proteins that share homology with their founding member fork head protein, Drosophila.
Cells contained in the bone marrow including fat cells (see ADIPOCYTES); STROMAL CELLS; MEGAKARYOCYTES; and the immediate precursors of most blood cells.
A group of genetically identical cells all descended from a single common ancestral cell by mitosis in eukaryotes or by binary fission in prokaryotes. Clone cells also include populations of recombinant DNA molecules all carrying the same inserted sequence. (From King & Stansfield, Dictionary of Genetics, 4th ed)
A classification of lymphocytes based on structurally or functionally different populations of cells.
A soluble factor produced by activated T-LYMPHOCYTES that induces the expression of MHC CLASS II GENES and FC RECEPTORS on B-LYMPHOCYTES and causes their proliferation and differentiation. It also acts on T-lymphocytes, MAST CELLS, and several other hematopoietic lineage cells.
Includes the spectrum of human immunodeficiency virus infections that range from asymptomatic seropositivity, thru AIDS-related complex (ARC), to acquired immunodeficiency syndrome (AIDS).
A classification of T-lymphocytes, especially into helper/inducer, suppressor/effector, and cytotoxic subsets, based on structurally or functionally different populations of cells.
Mice homozygous for the mutant autosomal recessive gene "scid" which is located on the centromeric end of chromosome 16. These mice lack mature, functional lymphocytes and are thus highly susceptible to lethal opportunistic infections if not chronically treated with antibiotics. The lack of B- and T-cell immunity resembles severe combined immunodeficiency (SCID) syndrome in human infants. SCID mice are useful as animal models since they are receptive to implantation of a human immune system producing SCID-human (SCID-hu) hematochimeric mice.
The degree of similarity between sequences of amino acids. This information is useful for the analyzing genetic relatedness of proteins and species.
Quantitative determination of receptor (binding) proteins in body fluids or tissue using radioactively labeled binding reagents (e.g., antibodies, intracellular receptors, plasma binders).
Antigens on surfaces of cells, including infectious or foreign cells or viruses. They are usually protein-containing groups on cell membranes or walls and may be isolated.
Mature LYMPHOCYTES and MONOCYTES transported by the blood to the body's extravascular space. They are morphologically distinguishable from mature granulocytic leukocytes by their large, non-lobed nuclei and lack of coarse, heavily stained cytoplasmic granules.
A lectin and cell adhesion molecule found in B-LYMPHOCYTES. It interacts with SIALIC ACIDS and mediates signaling from B-CELL ANTIGEN RECEPTORS.
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.
Cell surface glycoproteins that bind to chemokines and thus mediate the migration of pro-inflammatory molecules. The receptors are members of the seven-transmembrane G protein-coupled receptor family. Like the CHEMOKINES themselves, the receptors can be divided into at least three structural branches: CR, CCR, and CXCR, according to variations in a shared cysteine motif.
A membrane-bound or cytosolic enzyme that catalyzes the synthesis of CYCLIC ADP-RIBOSE (cADPR) from nicotinamide adenine dinucleotide (NAD). This enzyme generally catalyzes the hydrolysis of cADPR to ADP-RIBOSE, as well, and sometimes the synthesis of cyclic ADP-ribose 2' phosphate (2'-P-cADPR) from NADP.
Linear POLYPEPTIDES that are synthesized on RIBOSOMES and may be further modified, crosslinked, cleaved, or assembled into complex proteins with several subunits. The specific sequence of AMINO ACIDS determines the shape the polypeptide will take, during PROTEIN FOLDING, and the function of the protein.
The largest family of cell surface receptors involved in SIGNAL TRANSDUCTION. They share a common structure and signal through HETEROTRIMERIC G-PROTEINS.
The specific failure of a normally responsive individual to make an immune response to a known antigen. It results from previous contact with the antigen by an immunologically immature individual (fetus or neonate) or by an adult exposed to extreme high-dose or low-dose antigen, or by exposure to radiation, antimetabolites, antilymphocytic serum, etc.
The relationship between the dose of an administered drug and the response of the organism to the drug.
Membrane antigens associated with maturation stages of B-lymphocytes, often expressed in tumors of B-cell origin.
The ability of a substance to be dissolved, i.e. to form a solution with another substance. (From McGraw-Hill Dictionary of Scientific and Technical Terms, 6th ed)
They are oval or bean shaped bodies (1 - 30 mm in diameter) located along the lymphatic system.
Peptides composed of between two and twelve amino acids.
Intracellular receptors that can be found in the cytoplasm or in the nucleus. They bind to extracellular signaling molecules that migrate through or are transported across the CELL MEMBRANE. Many members of this class of receptors occur in the cytoplasm and are transported to the CELL NUCLEUS upon ligand-binding where they signal via DNA-binding and transcription regulation. Also included in this category are receptors found on INTRACELLULAR MEMBRANES that act via mechanisms similar to CELL SURFACE RECEPTORS.
The introduction of a phosphoryl group into a compound through the formation of an ester bond between the compound and a phosphorus moiety.
Subset of helper-inducer T-lymphocytes which synthesize and secrete interleukin-2, gamma-interferon, and interleukin-12. Due to their ability to kill antigen-presenting cells and their lymphokine-mediated effector activity, Th1 cells are associated with vigorous delayed-type hypersensitivity reactions.
Any of several ways in which living cells of an organism communicate with one another, whether by direct contact between cells or by means of chemical signals carried by neurotransmitter substances, hormones, and cyclic AMP.
Membrane glycoproteins consisting of an alpha subunit and a BETA 2-MICROGLOBULIN beta subunit. In humans, highly polymorphic genes on CHROMOSOME 6 encode the alpha subunits of class I antigens and play an important role in determining the serological specificity of the surface antigen. Class I antigens are found on most nucleated cells and are generally detected by their reactivity with alloantisera. These antigens are recognized during GRAFT REJECTION and restrict cell-mediated lysis of virus-infected cells.
Regulatory proteins and peptides that are signaling molecules involved in the process of PARACRINE COMMUNICATION. They are generally considered factors that are expressed by one cell and are responded to by receptors on another nearby cell. They are distinguished from HORMONES in that their actions are local rather than distal.
The process by which two molecules of the same chemical composition form a condensation product or polymer.
Specific molecular sites on the surface of various cells, including B-lymphocytes and macrophages, that combine with IMMUNOGLOBULIN Gs. Three subclasses exist: Fc gamma RI (the CD64 antigen, a low affinity receptor), Fc gamma RII (the CD32 antigen, a high affinity receptor), and Fc gamma RIII (the CD16 antigen, a low affinity receptor).
An adhesion-promoting leukocyte surface membrane heterodimer. The alpha subunit consists of the CD11b ANTIGEN and the beta subunit the CD18 ANTIGEN. The antigen, which is an integrin, functions both as a receptor for complement 3 and in cell-cell and cell-substrate adhesive interactions.
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.
Theoretical representations that simulate the behavior or activity of biological processes or diseases. For disease models in living animals, DISEASE MODELS, ANIMAL is available. Biological models include the use of mathematical equations, computers, and other electronic equipment.
Antibodies that inhibit the reaction between ANTIGEN and other antibodies or sensitized T-LYMPHOCYTES (e.g., antibodies of the IMMUNOGLOBULIN G class that compete with IGE antibodies for antigen, thereby blocking an allergic response). Blocking antibodies that bind tumors and prevent destruction of tumor cells by CYTOTOXIC T-LYMPHOCYTES have also been called enhancing antibodies. (Rosen et al., Dictionary of Immunology, 1989)
Short sequences (generally about 10 base pairs) of DNA that are complementary to sequences of messenger RNA and allow reverse transcriptases to start copying the adjacent sequences of mRNA. Primers are used extensively in genetic and molecular biology techniques.
The level of protein structure in which regular hydrogen-bond interactions within contiguous stretches of polypeptide chain give rise to alpha helices, beta strands (which align to form beta sheets) or other types of coils. This is the first folding level of protein conformation.
CELL LINES derived from the CV-1 cell line by transformation with a replication origin defective mutant of SV40 VIRUS, which codes for wild type large T antigen (ANTIGENS, POLYOMAVIRUS TRANSFORMING). They are used for transfection and cloning. (The CV-1 cell line was derived from the kidney of an adult male African green monkey (CERCOPITHECUS AETHIOPS).)
A large group of proteins that control APOPTOSIS. This family of proteins includes many ONCOGENE PROTEINS as well as a wide variety of classes of INTRACELLULAR SIGNALING PEPTIDES AND PROTEINS such as CASPASES.
The process by which antigen is presented to lymphocytes in a form they can recognize. This is performed by antigen presenting cells (APCs). Some antigens require processing before they can be recognized. Antigen processing consists of ingestion and partial digestion of the antigen by the APC, followed by presentation of fragments on the cell surface. (From Rosen et al., Dictionary of Immunology, 1989)
The span of viability of a cell characterized by the capacity to perform certain functions such as metabolism, growth, reproduction, some form of responsiveness, and adaptability.
Large, transmembrane, non-covalently linked glycoproteins (alpha and beta). Both chains can be polymorphic although there is more structural variation in the beta chains. The class II antigens in humans are called HLA-D ANTIGENS and are coded by a gene on chromosome 6. In mice, two genes named IA and IE on chromosome 17 code for the H-2 antigens. The antigens are found on B-lymphocytes, macrophages, epidermal cells, and sperm and are thought to mediate the competence of and cellular cooperation in the immune response. The term IA antigens used to refer only to the proteins encoded by the IA genes in the mouse, but is now used as a generic term for any class II histocompatibility antigen.
A family of transmembrane glycoproteins (MEMBRANE GLYCOPROTEINS) consisting of noncovalent heterodimers. They interact with a wide variety of ligands including EXTRACELLULAR MATRIX PROTEINS; COMPLEMENT, and other cells, while their intracellular domains interact with the CYTOSKELETON. The integrins consist of at least three identified families: the cytoadhesin receptors(RECEPTORS, CYTOADHESIN), the leukocyte adhesion receptors (RECEPTORS, LEUKOCYTE ADHESION), and the VERY LATE ANTIGEN RECEPTORS. Each family contains a common beta-subunit (INTEGRIN BETA CHAINS) combined with one or more distinct alpha-subunits (INTEGRIN ALPHA CHAINS). These receptors participate in cell-matrix and cell-cell adhesion in many physiologically important processes, including embryological development; HEMOSTASIS; THROMBOSIS; WOUND HEALING; immune and nonimmune defense mechanisms; and oncogenic transformation.
Endogenous substances, usually proteins, which are effective in the initiation, stimulation, or termination of the genetic transcription process.

Reciprocal control of T helper cell and dendritic cell differentiation. (1/1953)

It is not known whether subsets of dendritic cells provide different cytokine microenvironments that determine the differentiation of either type-1 T helper (TH1) or TH2 cells. Human monocyte (pDC1)-derived dendritic cells (DC1) were found to induce TH1 differentiation, whereas dendritic cells (DC2) derived from CD4+CD3-CD11c- plasmacytoid cells (pDC2) induced TH2 differentiation by use of a mechanism unaffected by interleukin-4 (IL-4) or IL-12. The TH2 cytokine IL-4 enhanced DC1 maturation and killed pDC2, an effect potentiated by IL-10 but blocked by CD40 ligand and interferon-gamma. Thus, a negative feedback loop from the mature T helper cells may selectively inhibit prolonged TH1 or TH2 responses by regulating survival of the appropriate dendritic cell subset.  (+info)

Expression of stromelysin-3 in atherosclerotic lesions: regulation via CD40-CD40 ligand signaling in vitro and in vivo. (2/1953)

Stromelysin-3 is an unusual matrix metalloproteinase, being released in the active rather than zymogen form and having a distinct substrate specificity, targeting serine proteinase inhibitors (serpins), which regulate cellular functions involved in atherosclerosis. We report here that human atherosclerotic plaques (n = 7) express stromelysin-3 in situ, whereas fatty streaks (n = 5) and normal arterial specimens (n = 5) contain little or no stromelysin-3. Stromelysin-3 mRNA and protein colocalized with endothelial cells, smooth muscle cells, and macrophages within the lesion. In vitro, usual inducers of matrix metalloproteinases such as interleukin-1, interferon-gamma, or tumor necrosis factor alpha did not augment stromelysin-3 in vascular wall cells. However, T cell-derived as well as recombinant CD40 ligand (CD40L, CD154), an inflammatory mediator recently localized in atheroma, induced de novo synthesis of stromelysin-3. In addition, stromelysin-3 mRNA and protein colocalized with CD40L and CD40 within atheroma. In accordance with the in situ and in vitro data obtained with human material, interruption of the CD40-CD40L signaling pathway in low density lipoprotein receptor-deficient hyperlipidemic mice substantially decreased expression of the enzyme within atherosclerotic plaques. These observations establish the expression of the unusual matrix metalloproteinase stromelysin-3 in human atherosclerotic lesions and implicate CD40-CD40L signaling in its regulation, thus providing a possible new pathway that triggers complications within atherosclerotic lesions.  (+info)

Minimal cross-linking and epitope requirements for CD40-dependent suppression of apoptosis contrast with those for promotion of the cell cycle and homotypic adhesions in human B cells. (3/1953)

Eight different CD40 mAb shared with soluble trimeric CD40 ligand (sCD40LT) the capacity to rescue germinal center (GC) B cells from spontaneous apoptosis and to suppress antigen receptor-driven apoptosis in group I Burkitt's lymphoma cells. Three mAb (G28-5, M2 and M3) mimicked sCD40LT in its ability to promote strong homotypic adhesion in resting B cells, whereas others (EA5, BL-OGY/C4 and 5C3) failed to stimulate strong clustering. Binding studies revealed that only those mAb that promoted strong B cell clustering bound at, or near to, the CD40L binding site. While all eight mAb and sCD40LT were capable of synergizing with IL-4 or phorbol ester for promoting DNA synthesis in resting B cells, co-stimulus-independent activation of the cells into cycle through CD40 related directly to the extent of receptor cross-linking. Thus, mAb which bound outside the CD40L binding site synergized with sCD40LT for promoting DNA synthesis; maximal levels of stimulation were achieved by presenting any of the mAb on CD32 transfectants in the absence of sCD40LT or by cross-linking bound sCD40LT with a second antibody. Monomeric sCD40L, which was able to promote rescue of GC B cells from apoptosis, was unable to drive resting B cells into cycle. These studies demonstrate that CD40-dependent rescue of human B cells from apoptosis requires minimal cross-linking and is essentially epitope independent, whereas the requirements for promoting cell cycle progression and homotypic adhesion are more stringent. Possible mechanisms underlying these differences and their physiological significance are discussed.  (+info)

TRANCE, a TNF family member, is differentially expressed on T cell subsets and induces cytokine production in dendritic cells. (4/1953)

TNF-related activation-induced cytokine (TRANCE) is a member of the TNF family recently identified in activated T cells. We report here that TRANCE mRNA is constitutively expressed in memory, but not naive, T cells and in single-positive thymocytes. Upon TCR/CD3 stimulation, TRANCE mRNA and surface protein expression are rapidly up-regulated in CD4+ and CD8+ T cells, which can be further enhanced on CD4+ T cells by CD28-mediated costimulation. However, TRANCE induction is significantly suppressed when cells are stimulated in the presence of IL-4, but is not modified in the presence of IFN-alpha, IFN-gamma, TGF-beta, TNF-alpha, or IL-2. High levels of TRANCE receptor expression are found on mature dendritic cells (DCs). In this study we show that activated T and B cells also express TRANCE receptor, but only at low levels. TRANCE, however, does not exert any significant effect on the proliferation, activation, or survival of those cells. In DCs, TRANCE induces the expression of proinflammatory cytokines (IL-6, IL-1) and T cell growth and differentiation factors (IL-12, IL-15) in addition to enhancing DC survival. Moreover, TRANCE cooperates with CD40 ligand or TNF-alpha to further increase the viability of DCs, suggesting that several TNF-related molecules on activated T cells may cooperatively regulate the function and survival of DCs to enhance T cell-mediated immune responses.  (+info)

N-acetyl-L-cysteine inhibits primary human T cell responses at the dendritic cell level: association with NF-kappaB inhibition. (5/1953)

N-acetyl-L-cysteine (NAC) is an antioxidant molecule endowed with immunomodulatory properties. To investigate the effect of NAC on the induction phase of T cell responses, we analyzed its action on human dendritic cells (DC) derived from adherent PBMC cultured with IL-4 and granulocyte-macrophage CSF. We first found that NAC inhibited the constitutive as well as the LPS-induced activity of the transcription factor NF-kappaB. In parallel, NAC was shown to down-regulate the production of cytokines by DC as well as their surface expression of HLA-DR, CD86 (B7-2), and CD40 molecules both at the basal state and upon LPS activation. NAC also inhibited DC responses induced by CD40 engagement. The inhibitory effects of NAC were not due to nonspecific toxicity as neither the viability of DC nor their mannose receptor-mediated endocytosis were modified by NAC. Finally, we found that the addition of NAC to MLR between naive T cells and allogeneic DC resulted in a profound inhibition of alloreactive responses, which could be attributed to a defect of DC as APC-independent T cell responses were not inhibited by NAC. Altogether, our results suggest that NAC might impair the generation of primary immune responses in humans through its inhibitory action on DC.  (+info)

Lymphocyte activation gene-3, a MHC class II ligand expressed on activated T cells, stimulates TNF-alpha and IL-12 production by monocytes and dendritic cells. (6/1953)

Lymphocyte activation gene-3 (LAG-3) is an MHC class II ligand structurally and genetically related to CD4. Although its expression is restricted to activated T cells and NK cells, the functions of LAG-3 remain to be elucidated. Here, we report on the expression and function of LAG-3 on proinflammatory bystander T cells that are activated in the absence of TCR engagement. LAG-3 is expressed at high levels on human T cells cocultured with autologous monocytes and IL-2 and synergizes with the low levels of CD40 ligand (CD40L) expressed on these cells to trigger TNF-alpha and IL-12 production by monocytes. Indeed, anti-LAG-3 mAb inhibits both IL-12 and IFN-gamma production in IL-2-stimulated cocultures of T cells and autologous monocytes. Soluble LAG-3Ig fusion protein markedly enhances IL-12 production by monocytes stimulated with infra-optimal concentrations of sCD40L, whereas it directly stimulates monocyte-derived dendritic cells (DC) for the production of TNF-alpha and IL-12, unravelling an enhanced responsiveness to MHC class II engagemenent in DC as compared with activated monocytes. Thus similar to CD40L, LAG-3 may be involved in the proinflammatory activity of cytokine-activated bystander T cells and most importantly it may directly activate DC.  (+info)

Regulation of interleukin (IL)-12 receptor beta2 subunit expression by endogenous IL-12: a critical step in the differentiation of pathogenic autoreactive T cells. (7/1953)

The interleukin (IL)-12 receptor (R)beta2 subunit is the critical molecule involved in maintaining IL-12 responsiveness and controlling T helper cell type 1 lineage commitment. We demonstrate that IL-12 and interferon (IFN)-gamma play separate, but complementary, roles in regulating IL-12Rbeta2 expression on antigen-specific CD4(+) T cells. These results are consistent with our previous observation that IL-12 can promote autoimmune disease through IFN-gamma-independent as well as -dependent pathways. Therefore, we compared the induction of IL-12 by, and the expression of the IL-12Rbeta2 subunit on, myelin basic protein (MBP)-specific T cells from experimental allergic encephalomyelitis (EAE)-susceptible SJL (H-2(s)) mice and from EAE- resistant B10.S mice (H-2(s)). B10.S mice had an antigen-specific defect in their capacity to upregulate the IL-12Rbeta2 subunit. Defective expression was not secondary to the production of suppressive cytokines, but to a failure of B10.S MBP-specific T cells to upregulate CD40 ligand expression and to induce the production of IL-12. IL-12Rbeta2 expression as well as encephalitogenicity of these cells could be restored by the addition of IL-12. These results suggest that the development of immunotherapies that target the IL-12Rbeta2 subunit may be useful for the treatment of autoimmune diseases.  (+info)

Bone marrow-derived cells are required for the induction of a pulmonary inflammatory response mediated by CD40 ligation. (8/1953)

The expression of inflammatory mediators by various cells following in vitro CD40 ligation is well known. However, knowledge of the role and interaction with these cells in the establishment and maintenance of in vivo immune-mediated inflammation is limited. In this report, a chimeric mouse model based on CD40 knockout and wild-type mice was used to assess the role of bone marrow (BM)-derived and non-BM-derived cells in a CD40-mediated pulmonary inflammation response. CD40+ BM-derived cells were required for initial cell recruitment, pulmonary edema, and weight loss associated with this response. The structural CD40+ non-BM-derived cells of the lung, such as fibroblasts, epithelial cells, and endothelial cells, could not by themselves establish any level of pulmonary inflammation. However, both the CD40+ BM-derived cells and the structural CD40+ non-BM-derived cells of the lung were required to maximize the level of pulmonary inflammation. Both B cells and T cells played a contributing role in macrophage recruitment and pulmonary edema but neither contributed to the inflammation-associated weight loss. These experiments indicate that CD40+ BM-derived cells were critical to the induction of pulmonary inflammation and that alveolar macrophages, B cells, and T cells contributed to selective aspects of the response.  (+info)

HIV (human immunodeficiency virus) infection is a condition in which the body is infected with HIV, a type of retrovirus that attacks the body's immune system. HIV infection can lead to AIDS (acquired immunodeficiency syndrome), a condition in which the immune system is severely damaged and the body is unable to fight off infections and diseases.

There are several ways that HIV can be transmitted, including:

1. Sexual contact with an infected person
2. Sharing of needles or other drug paraphernalia with an infected person
3. Mother-to-child transmission during pregnancy, childbirth, or breastfeeding
4. Blood transfusions ( although this is rare in developed countries due to screening processes)
5. Organ transplantation (again, rare)

The symptoms of HIV infection can be mild at first and may not appear until several years after infection. These symptoms can include:

1. Fever
2. Fatigue
3. Swollen glands in the neck, armpits, and groin
4. Rash
5. Muscle aches and joint pain
6. Night sweats
7. Diarrhea
8. Weight loss

If left untreated, HIV infection can progress to AIDS, which is a life-threatening condition that can cause a wide range of symptoms, including:

1. Opportunistic infections (such as pneumocystis pneumonia)
2. Cancer (such as Kaposi's sarcoma)
3. Wasting syndrome
4. Neurological problems (such as dementia and seizures)

HIV infection is diagnosed through a combination of blood tests and physical examination. Treatment typically involves antiretroviral therapy (ART), which is a combination of medications that work together to suppress the virus and slow the progression of the disease.

Prevention methods for HIV infection include:

1. Safe sex practices, such as using condoms and dental dams
2. Avoiding sharing needles or other drug-injecting equipment
3. Avoiding mother-to-child transmission during pregnancy, childbirth, or breastfeeding
4. Post-exposure prophylaxis (PEP), which is a short-term treatment that can prevent infection after potential exposure to the virus
5. Pre-exposure prophylaxis (PrEP), which is a daily medication that can prevent infection in people who are at high risk of being exposed to the virus.

It's important to note that HIV infection is manageable with proper treatment and care, and that people living with HIV can lead long and healthy lives. However, it's important to be aware of the risks and take steps to prevent transmission.

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.

There are several key features of inflammation:

1. Increased blood flow: Blood vessels in the affected area dilate, allowing more blood to flow into the tissue and bringing with it immune cells, nutrients, and other signaling molecules.
2. Leukocyte migration: White blood cells, such as neutrophils and monocytes, migrate towards the site of inflammation in response to chemical signals.
3. Release of mediators: Inflammatory mediators, such as cytokines and chemokines, are released by immune cells and other cells in the affected tissue. These molecules help to coordinate the immune response and attract more immune cells to the site of inflammation.
4. Activation of immune cells: Immune cells, such as macrophages and T cells, become activated and start to phagocytose (engulf) pathogens or damaged tissue.
5. Increased heat production: Inflammation can cause an increase in metabolic activity in the affected tissue, leading to increased heat production.
6. Redness and swelling: Increased blood flow and leakiness of blood vessels can cause redness and swelling in the affected area.
7. Pain: Inflammation can cause pain through the activation of nociceptors (pain-sensing neurons) and the release of pro-inflammatory mediators.

Inflammation can be acute or chronic. Acute inflammation is a short-term response to injury or infection, which helps to resolve the issue quickly. Chronic inflammation is a long-term response that can cause ongoing damage and diseases such as arthritis, asthma, and cancer.

There are several types of inflammation, including:

1. Acute inflammation: A short-term response to injury or infection.
2. Chronic inflammation: A long-term response that can cause ongoing damage and diseases.
3. Autoimmune inflammation: An inappropriate immune response against the body's own tissues.
4. Allergic inflammation: An immune response to a harmless substance, such as pollen or dust mites.
5. Parasitic inflammation: An immune response to parasites, such as worms or fungi.
6. Bacterial inflammation: An immune response to bacteria.
7. Viral inflammation: An immune response to viruses.
8. Fungal inflammation: An immune response to fungi.

There are several ways to reduce inflammation, including:

1. Medications such as nonsteroidal anti-inflammatory drugs (NSAIDs), corticosteroids, and disease-modifying anti-rheumatic drugs (DMARDs).
2. Lifestyle changes, such as a healthy diet, regular exercise, stress management, and getting enough sleep.
3. Alternative therapies, such as acupuncture, herbal supplements, and mind-body practices.
4. Addressing underlying conditions, such as hormonal imbalances, gut health issues, and chronic infections.
5. Using anti-inflammatory compounds found in certain foods, such as omega-3 fatty acids, turmeric, and ginger.

It's important to note that chronic inflammation can lead to a range of health problems, including:

1. Arthritis
2. Diabetes
3. Heart disease
4. Cancer
5. Alzheimer's disease
6. Parkinson's disease
7. Autoimmune disorders, such as lupus and rheumatoid arthritis.

Therefore, it's important to manage inflammation effectively to prevent these complications and improve overall health and well-being.

There are several possible causes of lymphopenia, including:

1. Viral infections: Many viral infections can cause lymphopenia, such as HIV/AIDS, hepatitis B and C, and influenza.
2. Bacterial infections: Some bacterial infections, such as tuberculosis and leprosy, can also cause lymphopenia.
3. Cancer: Certain types of cancer, such as Hodgkin's disease and non-Hodgkin's lymphoma, can cause lymphopenia by destroying lymphocytes.
4. Autoimmune disorders: Autoimmune disorders, such as rheumatoid arthritis and lupus, can cause lymphopenia by attacking the body's own tissues, including lymphocytes.
5. Radiation therapy: Radiation therapy can destroy lymphocytes and cause lymphopenia.
6. Medications: Certain medications, such as chemotherapy drugs and antibiotics, can cause lymphopenia as a side effect.
7. Genetic disorders: Some genetic disorders, such as X-linked lymphoproliferative disease, can cause lymphopenia by affecting the development or function of lymphocytes.

Symptoms of lymphopenia can include recurring infections, fatigue, and swollen lymph nodes. Treatment of lymphopenia depends on the underlying cause and may involve antibiotics, antiviral medications, or immunoglobulin replacement therapy. In some cases, a bone marrow transplant may be necessary.

Overall, lymphopenia is a condition that can have a significant impact on quality of life, and it is important to seek medical attention if symptoms persist or worsen over time. With proper diagnosis and treatment, many people with lymphopenia can experience improved health outcomes and a better quality of life.

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.

Neoplasm refers to an abnormal growth of cells that can be benign (non-cancerous) or malignant (cancerous). Neoplasms can occur in any part of the body and can affect various organs and tissues. The term "neoplasm" is often used interchangeably with "tumor," but while all tumors are neoplasms, not all neoplasms are tumors.

Types of Neoplasms

There are many different types of neoplasms, including:

1. Carcinomas: These are malignant tumors that arise in the epithelial cells lining organs and glands. Examples include breast cancer, lung cancer, and colon cancer.
2. Sarcomas: These are malignant tumors that arise in connective tissue, such as bone, cartilage, and fat. Examples include osteosarcoma (bone cancer) and soft tissue sarcoma.
3. Lymphomas: These are cancers of the immune system, specifically affecting the lymph nodes and other lymphoid tissues. Examples include Hodgkin lymphoma and non-Hodgkin lymphoma.
4. Leukemias: These are cancers of the blood and bone marrow that affect the white blood cells. Examples include acute myeloid leukemia (AML) and chronic lymphocytic leukemia (CLL).
5. Melanomas: These are malignant tumors that arise in the pigment-producing cells called melanocytes. Examples include skin melanoma and eye melanoma.

Causes and Risk Factors of Neoplasms

The exact causes of neoplasms are not fully understood, but there are several known risk factors that can increase the likelihood of developing a neoplasm. These include:

1. Genetic predisposition: Some people may be born with genetic mutations that increase their risk of developing certain types of neoplasms.
2. Environmental factors: Exposure to certain environmental toxins, such as radiation and certain chemicals, can increase the risk of developing a neoplasm.
3. Infection: Some neoplasms are caused by viruses or bacteria. For example, human papillomavirus (HPV) is a common cause of cervical cancer.
4. Lifestyle factors: Factors such as smoking, excessive alcohol consumption, and a poor diet can increase the risk of developing certain types of neoplasms.
5. Family history: A person's risk of developing a neoplasm may be higher if they have a family history of the condition.

Signs and Symptoms of Neoplasms

The signs and symptoms of neoplasms can vary depending on the type of cancer and where it is located in the body. Some common signs and symptoms include:

1. Unusual lumps or swelling
2. Pain
3. Fatigue
4. Weight loss
5. Change in bowel or bladder habits
6. Unexplained bleeding
7. Coughing up blood
8. Hoarseness or a persistent cough
9. Changes in appetite or digestion
10. Skin changes, such as a new mole or a change in the size or color of an existing mole.

Diagnosis and Treatment of Neoplasms

The diagnosis of a neoplasm usually involves a combination of physical examination, imaging tests (such as X-rays, CT scans, or MRI scans), and biopsy. A biopsy involves removing a small sample of tissue from the suspected tumor and examining it under a microscope for cancer cells.

The treatment of neoplasms depends on the type, size, location, and stage of the cancer, as well as the patient's overall health. Some common treatments include:

1. Surgery: Removing the tumor and surrounding tissue can be an effective way to treat many types of cancer.
2. Chemotherapy: Using drugs to kill cancer cells can be effective for some types of cancer, especially if the cancer has spread to other parts of the body.
3. Radiation therapy: Using high-energy radiation to kill cancer cells can be effective for some types of cancer, especially if the cancer is located in a specific area of the body.
4. Immunotherapy: Boosting the body's immune system to fight cancer can be an effective treatment for some types of cancer.
5. Targeted therapy: Using drugs or other substances to target specific molecules on cancer cells can be an effective treatment for some types of cancer.

Prevention of Neoplasms

While it is not always possible to prevent neoplasms, there are several steps that can reduce the risk of developing cancer. These include:

1. Avoiding exposure to known carcinogens (such as tobacco smoke and radiation)
2. Maintaining a healthy diet and lifestyle
3. Getting regular exercise
4. Not smoking or using tobacco products
5. Limiting alcohol consumption
6. Getting vaccinated against certain viruses that are associated with cancer (such as human papillomavirus, or HPV)
7. Participating in screening programs for early detection of cancer (such as mammograms for breast cancer and colonoscopies for colon cancer)
8. Avoiding excessive exposure to sunlight and using protective measures such as sunscreen and hats to prevent skin cancer.

It's important to note that not all cancers can be prevented, and some may be caused by factors that are not yet understood or cannot be controlled. However, by taking these steps, individuals can reduce their risk of developing cancer and improve their overall health and well-being.

Disease progression can be classified into several types based on the pattern of worsening:

1. Chronic progressive disease: In this type, the disease worsens steadily over time, with a gradual increase in symptoms and decline in function. Examples include rheumatoid arthritis, osteoarthritis, and Parkinson's disease.
2. Acute progressive disease: This type of disease worsens rapidly over a short period, often followed by periods of stability. Examples include sepsis, acute myocardial infarction (heart attack), and stroke.
3. Cyclical disease: In this type, the disease follows a cycle of worsening and improvement, with periodic exacerbations and remissions. Examples include multiple sclerosis, lupus, and rheumatoid arthritis.
4. Recurrent disease: This type is characterized by episodes of worsening followed by periods of recovery. Examples include migraine headaches, asthma, and appendicitis.
5. Catastrophic disease: In this type, the disease progresses rapidly and unpredictably, with a poor prognosis. Examples include cancer, AIDS, and organ failure.

Disease progression can be influenced by various factors, including:

1. Genetics: Some diseases are inherited and may have a predetermined course of progression.
2. Lifestyle: Factors such as smoking, lack of exercise, and poor diet can contribute to disease progression.
3. Environmental factors: Exposure to toxins, allergens, and other environmental stressors can influence disease progression.
4. Medical treatment: The effectiveness of medical treatment can impact disease progression, either by slowing or halting the disease process or by causing unintended side effects.
5. Co-morbidities: The presence of multiple diseases or conditions can interact and affect each other's progression.

Understanding the type and factors influencing disease progression is essential for developing effective treatment plans and improving patient outcomes.

There are several types of melanoma, including:

1. Superficial spreading melanoma: This is the most common type of melanoma, accounting for about 70% of cases. It usually appears as a flat or slightly raised discolored patch on the skin.
2. Nodular melanoma: This type of melanoma is more aggressive and accounts for about 15% of cases. It typically appears as a raised bump on the skin, often with a darker color.
3. Acral lentiginous melanoma: This type of melanoma affects the palms of the hands, soles of the feet, or nail beds and accounts for about 5% of cases.
4. Lentigo maligna melanoma: This type of melanoma usually affects the face and is more common in older adults.

The risk factors for developing melanoma include:

1. Ultraviolet (UV) radiation exposure from the sun or tanning beds
2. Fair skin, light hair, and light eyes
3. A history of sunburns
4. Weakened immune system
5. Family history of melanoma

The symptoms of melanoma can vary depending on the type and location of the cancer. Common symptoms include:

1. Changes in the size, shape, or color of a mole
2. A new mole or growth on the skin
3. A spot or sore that bleeds or crusts over
4. Itching or pain on the skin
5. Redness or swelling around a mole

If melanoma is suspected, a biopsy will be performed to confirm the diagnosis. Treatment options for melanoma depend on the stage and location of the cancer and may include surgery, chemotherapy, radiation therapy, or a combination of these. Early detection and treatment are key to successful outcomes in melanoma cases.

In conclusion, melanoma is a type of skin cancer that can be deadly if not detected early. It is important to practice sun safety, perform regular self-exams, and seek medical attention if any suspicious changes are noticed on the skin. By being aware of the risk factors, symptoms, and treatment options for melanoma, individuals can take steps to protect themselves from this potentially deadly disease.

In LLCB, the B cells undergo a mutation that causes them to become cancerous and multiply rapidly. This can lead to an overproduction of these cells in the bone marrow, causing the bone marrow to become crowded and unable to produce healthy red blood cells, platelets, and white blood cells.

LLCB is typically a slow-growing cancer, and it can take years for symptoms to develop. However, as the cancer progresses, it can lead to a range of symptoms including fatigue, weakness, weight loss, fever, night sweats, and swollen lymph nodes.

LLCB is typically diagnosed through a combination of physical examination, blood tests, bone marrow biopsy, and imaging studies such as X-rays or CT scans. Treatment options for LLCB include chemotherapy, radiation therapy, and in some cases, stem cell transplantation.

Overall, while LLCB is a serious condition, it is typically slow-growing and can be managed with appropriate treatment. With current treatments, many people with LLCB can achieve long-term remission and a good quality of life.

There are several subtypes of lymphoma, B-cell, including:

1. Diffuse large B-cell lymphoma (DLBCL): This is the most common type of B-cell lymphoma and typically affects older adults.
2. Follicular lymphoma: This type of lymphoma grows slowly and often does not require treatment for several years.
3. Marginal zone lymphoma: This type of lymphoma develops in the marginal zone of the spleen or other lymphoid tissues.
4. Hodgkin lymphoma: This is a type of B-cell lymphoma that is characterized by the presence of Reed-Sternberg cells, which are abnormal cells that can be identified under a microscope.

The symptoms of lymphoma, B-cell can vary depending on the subtype and the location of the tumor. Common symptoms include swollen lymph nodes, fatigue, fever, night sweats, and weight loss.

Treatment for lymphoma, B-cell usually involves chemotherapy, which is a type of cancer treatment that uses drugs to kill cancer cells. Radiation therapy may also be used in some cases. In some cases, bone marrow or stem cell transplantation may be recommended.

Prognosis for lymphoma, B-cell depends on the subtype and the stage of the disease at the time of diagnosis. In general, the prognosis is good for patients with early-stage disease, but the cancer can be more difficult to treat if it has spread to other parts of the body.

Prevention of lymphoma, B-cell is not possible, as the exact cause of the disease is not known. However, avoiding exposure to certain risk factors, such as viral infections and pesticides, may help reduce the risk of developing the disease. Early detection and treatment can also improve outcomes for patients with lymphoma, B-cell.

Lymphoma, B-cell is a type of cancer that affects the immune system and can be treated with chemotherapy and other therapies. The prognosis varies depending on the subtype and stage of the disease at diagnosis. Prevention is not possible, but early detection and treatment can improve outcomes for patients with this condition.

2. Our research focuses on identifying the genetic mutations that contribute to experimental melanoma and developing targeted therapies.
3. The patient's experimental melanoma had spread to her lungs and liver, so we recommended chemotherapy and immunotherapy treatments.

Examples of acute diseases include:

1. Common cold and flu
2. Pneumonia and bronchitis
3. Appendicitis and other abdominal emergencies
4. Heart attacks and strokes
5. Asthma attacks and allergic reactions
6. Skin infections and cellulitis
7. Urinary tract infections
8. Sinusitis and meningitis
9. Gastroenteritis and food poisoning
10. Sprains, strains, and fractures.

Acute diseases can be treated effectively with antibiotics, medications, or other therapies. However, if left untreated, they can lead to chronic conditions or complications that may require long-term care. Therefore, it is important to seek medical attention promptly if symptoms persist or worsen over time.

* Peripheral T-cell lymphoma (PTCL): This is a rare type of T-cell lymphoma that can develop in the skin, lymph nodes, or other organs.
* Cutaneous T-cell lymphoma (CTCL): This is a type of PTCL that affects the skin and can cause lesions, rashes, and other skin changes.
* Anaplastic large cell lymphoma (ALCL): This is a rare subtype of PTCL that can develop in the lymph nodes, spleen, or bone marrow.
* Adult T-cell leukemia/lymphoma (ATLL): This is a rare and aggressive subtype of PTCL that is caused by the human T-lymphotropic virus type 1 (HTLV-1).

Symptoms of T-cell lymphoma can include:

* Swollen lymph nodes
* Fever
* Fatigue
* Weight loss
* Night sweats
* Skin lesions or rashes

Treatment options for T-cell lymphoma depend on the subtype and stage of the cancer, but may include:

* Chemotherapy
* Radiation therapy
* Immunotherapy
* Targeted therapy

Prognosis for T-cell lymphoma varies depending on the subtype and stage of the cancer, but in general, the prognosis for PTCL is poorer than for other types of non-Hodgkin lymphoma. However, with prompt and appropriate treatment, many people with T-cell lymphoma can achieve long-term remission or even be cured.

The symptoms of LCM can vary depending on the severity of the infection, but they typically include fever, headache, neck stiffness, and sensitivity to light. In severe cases, LCM can cause meningitis, encephalitis (inflammation of the brain), and even death.

The diagnosis of LCM is based on a combination of clinical symptoms, laboratory tests, and imaging studies such as MRI or CT scans. Laboratory tests may include blood tests to detect the presence of antibodies against the virus, as well as tests to assess liver function and other organ systems.

Treatment of LCM typically involves supportive care, such as intravenous fluids, oxygen therapy, and pain management. Antiviral medications may also be used in some cases. In severe cases, hospitalization may be required to monitor and treat the patient.

Prevention of LCM primarily involves avoiding contact with infected rodents, particularly during pregnancy and childhood when the risk of infection is higher. Good hygiene practices, such as frequent handwashing, can also help reduce the risk of transmission. Vaccines are not available for LCM, but research is ongoing to develop one.

The prognosis for LCM varies depending on the severity of the infection and the promptness and effectiveness of treatment. In general, the outcome is good for patients with mild symptoms, but those with severe infections may experience long-term neurological problems or death.

The disease is typically induced in laboratory animals such as mice or rats by immunizing them with myelin proteins, such as myelin basic protein (MBP) or proteolipid protein (PLP), emulsified in adjuvants. The resulting immune response leads to the production of autoantibodies and activated T cells that cross the blood-brain barrier and attack the CNS.

EAE is used as a model for MS because it shares many similarities with the human disease, including:

1. Demyelination: EAE induces demyelination of nerve fibers in the CNS, which is also a hallmark of MS.
2. Autoimmune response: The immune response in EAE is triggered by autoantigens, similar to MS.
3. Chronic course: EAE is a chronic disease with recurrent relapses, similar to MS.
4. Lesion distribution: EAE lesions are distributed throughout the CNS, including the cerebral cortex, cerebellum, brainstem, and spinal cord, which is also true for MS.

EAE has been used extensively in the study of MS to investigate the immunopathogenesis of the disease, to develop new diagnostic markers and treatments, and to test the efficacy of potential therapeutic agents.

Crohn disease can occur in any part of the GI tract, from the mouth to the anus, but it most commonly affects the ileum (the last portion of the small intestine) and the colon. The inflammation caused by Crohn disease can lead to the formation of scar tissue, which can cause narrowing or blockages in the intestines. This can lead to complications such as bowel obstruction or abscesses.

The exact cause of Crohn disease is not known, but it is believed to be an autoimmune disorder, meaning that the immune system mistakenly attacks healthy tissue in the GI tract. Genetic factors and environmental triggers such as smoking and diet also play a role in the development of the disease.

There is no cure for Crohn disease, but various treatments can help manage symptoms and prevent complications. These may include medications such as anti-inflammatory drugs, immunosuppressants, and biologics, as well as lifestyle changes such as dietary modifications and stress management techniques. In severe cases, surgery may be necessary to remove damaged portions of the GI tract.

Crohn disease can have a significant impact on quality of life, and it is important for individuals with the condition to work closely with their healthcare provider to manage their symptoms and prevent complications. With proper treatment and self-care, many people with Crohn disease are able to lead active and fulfilling lives.

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.

The symptoms of listeriosis can vary depending on the severity of the infection and the individual's overall health. Mild cases may present with flu-like symptoms, such as fever, headache, and muscle aches, while severe cases can lead to meningitis, encephalitis, and even death.

Diagnosis is typically made through a combination of physical examination, medical history, and laboratory tests, such as blood cultures or PCR (polymerase chain reaction) tests. Treatment typically involves antibiotics, and prompt treatment can significantly reduce the risk of serious complications and death.

Prevention measures include avoiding high-risk foods, such as soft cheeses and hot dogs, and maintaining good hygiene practices, such as washing hands and surfaces regularly. Vaccination against Listeria is not available, but efforts to improve food safety and sanitation can help reduce the risk of listeriosis outbreaks.

Overall, while listeriosis is a serious infection, prompt diagnosis and treatment can significantly improve outcomes for those affected.

The burden of chronic diseases is significant, with over 70% of deaths worldwide attributed to them, according to the World Health Organization (WHO). In addition to the physical and emotional toll they take on individuals and their families, chronic diseases also pose a significant economic burden, accounting for a large proportion of healthcare expenditure.

In this article, we will explore the definition and impact of chronic diseases, as well as strategies for managing and living with them. We will also discuss the importance of early detection and prevention, as well as the role of healthcare providers in addressing the needs of individuals with chronic diseases.

What is a Chronic Disease?

A chronic disease is a condition that lasts for an extended period of time, often affecting daily life and activities. Unlike acute diseases, which have a specific beginning and end, chronic diseases are long-term and persistent. Examples of chronic diseases include:

1. Diabetes
2. Heart disease
3. Arthritis
4. Asthma
5. Cancer
6. Chronic obstructive pulmonary disease (COPD)
7. Chronic kidney disease (CKD)
8. Hypertension
9. Osteoporosis
10. Stroke

Impact of Chronic Diseases

The burden of chronic diseases is significant, with over 70% of deaths worldwide attributed to them, according to the WHO. In addition to the physical and emotional toll they take on individuals and their families, chronic diseases also pose a significant economic burden, accounting for a large proportion of healthcare expenditure.

Chronic diseases can also have a significant impact on an individual's quality of life, limiting their ability to participate in activities they enjoy and affecting their relationships with family and friends. Moreover, the financial burden of chronic diseases can lead to poverty and reduce economic productivity, thus having a broader societal impact.

Addressing Chronic Diseases

Given the significant burden of chronic diseases, it is essential that we address them effectively. This requires a multi-faceted approach that includes:

1. Lifestyle modifications: Encouraging healthy behaviors such as regular physical activity, a balanced diet, and smoking cessation can help prevent and manage chronic diseases.
2. Early detection and diagnosis: Identifying risk factors and detecting diseases early can help prevent or delay their progression.
3. Medication management: Effective medication management is crucial for controlling symptoms and slowing disease progression.
4. Multi-disciplinary care: Collaboration between healthcare providers, patients, and families is essential for managing chronic diseases.
5. Health promotion and disease prevention: Educating individuals about the risks of chronic diseases and promoting healthy behaviors can help prevent their onset.
6. Addressing social determinants of health: Social determinants such as poverty, education, and employment can have a significant impact on health outcomes. Addressing these factors is essential for reducing health disparities and improving overall health.
7. Investing in healthcare infrastructure: Investing in healthcare infrastructure, technology, and research is necessary to improve disease detection, diagnosis, and treatment.
8. Encouraging policy change: Policy changes can help create supportive environments for healthy behaviors and reduce the burden of chronic diseases.
9. Increasing public awareness: Raising public awareness about the risks and consequences of chronic diseases can help individuals make informed decisions about their health.
10. Providing support for caregivers: Chronic diseases can have a significant impact on family members and caregivers, so providing them with support is essential for improving overall health outcomes.

Conclusion

Chronic diseases are a major public health burden that affect millions of people worldwide. Addressing these diseases requires a multi-faceted approach that includes lifestyle changes, addressing social determinants of health, investing in healthcare infrastructure, encouraging policy change, increasing public awareness, and providing support for caregivers. By taking a comprehensive approach to chronic disease prevention and management, we can improve the health and well-being of individuals and communities worldwide.

There are different types of Breast Neoplasms such as:

1. Fibroadenomas: These are benign tumors that are made up of glandular and fibrous tissues. They are usually small and round, with a smooth surface, and can be moved easily under the skin.

2. Cysts: These are fluid-filled sacs that can develop in both breast tissue and milk ducts. They are usually benign and can disappear on their own or be drained surgically.

3. Ductal Carcinoma In Situ (DCIS): This is a precancerous condition where abnormal cells grow inside the milk ducts. If left untreated, it can progress to invasive breast cancer.

4. Invasive Ductal Carcinoma (IDC): This is the most common type of breast cancer and starts in the milk ducts but grows out of them and invades surrounding tissue.

5. Invasive Lobular Carcinoma (ILC): It originates in the milk-producing glands (lobules) and grows out of them, invading nearby tissue.

Breast Neoplasms can cause various symptoms such as a lump or thickening in the breast or underarm area, skin changes like redness or dimpling, change in size or shape of one or both breasts, discharge from the nipple, and changes in the texture or color of the skin.

Treatment options for Breast Neoplasms may include surgery such as lumpectomy, mastectomy, or breast-conserving surgery, radiation therapy which uses high-energy beams to kill cancer cells, chemotherapy using drugs to kill cancer cells, targeted therapy which uses drugs or other substances to identify and attack cancer cells while minimizing harm to normal cells, hormone therapy, immunotherapy, and clinical trials.

It is important to note that not all Breast Neoplasms are cancerous; some are benign (non-cancerous) tumors that do not spread or grow.

The symptoms of AIDS can vary depending on the individual and the stage of the disease. Common symptoms include:

1. Fever
2. Fatigue
3. Swollen glands
4. Rash
5. Muscle aches and joint pain
6. Night sweats
7. Diarrhea
8. Weight loss
9. Memory loss and other neurological problems
10. Cancer and other opportunistic infections.

AIDS is diagnosed through blood tests that detect the presence of HIV antibodies or the virus itself. There is no cure for AIDS, but antiretroviral therapy (ART) can help manage the symptoms and slow the progression of the disease. Prevention methods include using condoms, pre-exposure prophylaxis (PrEP), and avoiding sharing needles or other injection equipment.

In summary, Acquired Immunodeficiency Syndrome (AIDS) is a severe and life-threatening condition caused by the Human Immunodeficiency Virus (HIV). It is characterized by a severely weakened immune system, which makes it difficult to fight off infections and diseases. While there is no cure for AIDS, antiretroviral therapy can help manage the symptoms and slow the progression of the disease. Prevention methods include using condoms, pre-exposure prophylaxis, and avoiding sharing needles or other injection equipment.

SAIDS was first identified in the 1980s in monkeys that were being used in research laboratories, and it has since been studied extensively as a model for HIV/AIDS research. Like HIV/AIDS, SAIDS is caused by the transmission of a virus from one animal to another through contact with infected bodily fluids, such as blood or semen.

The symptoms of SAIDS are similar to those of HIV/AIDS and include fever, fatigue, weight loss, and opportunistic infections. As the disease progresses, animals may also experience neurological symptoms, such as seizures and difficulty coordinating movements.

There is currently no cure for SAIDS, and treatment is focused on managing the symptoms and preventing complications. Research into the disease has led to a greater understanding of the immunopathogenesis of HIV/AIDS and has contributed to the development of new therapies for the disease.

SAIDS is important in medical research because it provides a valuable model for studying the immunopathogenesis of HIV/AIDS and for testing new therapies and vaccines. It also serves as a reminder of the importance of strict safety protocols when working with infectious agents, particularly in laboratory settings.

The most common type of colitis is ulcerative colitis, which affects the rectum and lower part of the colon. The symptoms of ulcerative colitis can include:

* Diarrhea (which may be bloody)
* Abdominal pain and cramping
* Rectal bleeding
* Weight loss
* Fever
* Loss of appetite
* Nausea and vomiting

Microscopic colitis is another type of colitis that is characterized by inflammation in the colon, but without visible ulcers or bleeding. The symptoms of microscopic colitis are similar to those of ulcerative colitis, but may be less severe.

Other types of colitis include:

* Infantile colitis: This is a rare condition that affects babies and young children, and is characterized by diarrhea, fever, and vomiting.
* Isomorphic colitis: This is a rare condition that affects the colon and rectum, and is characterized by inflammation and symptoms similar to ulcerative colitis.
* Radiation colitis: This is a condition that occurs after radiation therapy to the pelvic area, and is characterized by inflammation and symptoms similar to ulcerative colitis.
* Ischemic colitis: This is a condition where there is a reduction in blood flow to the colon, which can lead to inflammation and symptoms such as abdominal pain and diarrhea.

The diagnosis of colitis typically involves a combination of physical examination, medical history, and diagnostic tests such as:

* Colonoscopy: This is a test that uses a flexible tube with a camera on the end to visualize the inside of the colon and rectum.
* Endoscopy: This is a test that uses a flexible tube with a camera on the end to visualize the inside of the esophagus, stomach, and duodenum.
* Stool tests: These are tests that analyze stool samples for signs of inflammation or infection.
* Blood tests: These are tests that analyze blood samples for signs of inflammation or infection.
* Biopsy: This is a test that involves taking a small sample of tissue from the colon and examining it under a microscope for signs of inflammation or infection.

Treatment for colitis depends on the underlying cause, but may include medications such as:

* Aminosalicylates: These are medications that help to reduce inflammation in the colon and relieve symptoms such as diarrhea and abdominal pain. Examples include sulfasalazine (Azulfidine) and mesalamine (Asacol).
* Corticosteroids: These are medications that help to reduce inflammation in the body. They may be used short-term to control acute flares of colitis, or long-term to maintain remission. Examples include prednisone and hydrocortisone.
* Immunomodulators: These are medications that help to suppress the immune system and reduce inflammation. Examples include azathioprine (Imuran) and mercaptopurine (Purinethol).
* Biologics: These are medications that target specific proteins involved in the inflammatory response. Examples include infliximab (Remicade) and adalimumab (Humira).

In addition to medication, lifestyle changes such as dietary modifications and stress management techniques may also be helpful in managing colitis symptoms. Surgery may be necessary in some cases where the colitis is severe or persistent, and involves removing damaged portions of the colon and rectum.

It's important to note that colitis can increase the risk of developing colon cancer, so regular screening for colon cancer is recommended for people with chronic colitis. Additionally, people with colitis may be more susceptible to other health problems such as osteoporosis, osteopenia, and liver disease, so it's important to work closely with a healthcare provider to monitor for these conditions and take steps to prevent them.

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 colonic neoplasms, including:

1. Adenomas: These are benign growths that are usually precursors to colorectal cancer.
2. Carcinomas: These are malignant tumors that arise from the epithelial lining of the colon.
3. Sarcomas: These are rare malignant tumors that arise from the connective tissue of the colon.
4. Lymphomas: These are cancers of the immune system that can affect the colon.

Colonic neoplasms can cause a variety of symptoms, including bleeding, abdominal pain, and changes in bowel habits. They are often diagnosed through a combination of medical imaging tests (such as colonoscopy or CT scan) and biopsy. Treatment for colonic neoplasms depends on the type and stage of the tumor, and may include surgery, chemotherapy, and/or radiation therapy.

Overall, colonic neoplasms are a common condition that can have serious consequences if left untreated. It is important for individuals to be aware of their risk factors and to undergo regular screening for colon cancer to help detect and treat any abnormal growths or tumors in the colon.

Multiple myeloma is the second most common type of hematologic cancer after non-Hodgkin's lymphoma, accounting for approximately 1% of all cancer deaths worldwide. It is more common in older adults, with most patients being diagnosed over the age of 65.

The exact cause of multiple myeloma is not known, but it is believed to be linked to genetic mutations that occur in the plasma cells. There are several risk factors that have been associated with an increased risk of developing multiple myeloma, including:

1. Family history: Having a family history of multiple myeloma or other plasma cell disorders increases the risk of developing the disease.
2. Age: The risk of developing multiple myeloma increases with age, with most patients being diagnosed over the age of 65.
3. Race: African Americans are at higher risk of developing multiple myeloma than other races.
4. Obesity: Being overweight or obese may increase the risk of developing multiple myeloma.
5. Exposure to certain chemicals: Exposure to certain chemicals such as pesticides, solvents, and heavy metals has been linked to an increased risk of developing multiple myeloma.

The symptoms of multiple myeloma can vary depending on the severity of the disease and the organs affected. Common symptoms include:

1. Bone pain: Pain in the bones, particularly in the spine, ribs, or long bones, is a common symptom of multiple myeloma.
2. Fatigue: Feeling tired or weak is another common symptom of the disease.
3. Infections: Patients with multiple myeloma may be more susceptible to infections due to the impaired functioning of their immune system.
4. Bone fractures: Weakened bones can lead to an increased risk of fractures, particularly in the spine, hips, or ribs.
5. Kidney problems: Multiple myeloma can cause damage to the kidneys, leading to problems such as kidney failure or proteinuria (excess protein in the urine).
6. Anemia: A low red blood cell count can cause anemia, which can lead to fatigue, weakness, and shortness of breath.
7. Increased calcium levels: High levels of calcium in the blood can cause symptoms such as nausea, vomiting, constipation, and confusion.
8. Neurological problems: Multiple myeloma can cause neurological problems such as headaches, numbness or tingling in the arms and legs, and difficulty with coordination and balance.

The diagnosis of multiple myeloma typically involves a combination of physical examination, medical history, and laboratory tests. These may include:

1. Complete blood count (CBC): A CBC can help identify abnormalities in the numbers and characteristics of different types of blood cells, including red blood cells, white blood cells, and platelets.
2. Serum protein electrophoresis (SPEP): This test measures the levels of different proteins in the blood, including immunoglobulins (antibodies) and abnormal proteins produced by myeloma cells.
3. Urine protein electrophoresis (UPEP): This test measures the levels of different proteins in the urine.
4. Immunofixation: This test is used to identify the type of antibody produced by myeloma cells and to rule out other conditions that may cause similar symptoms.
5. Bone marrow biopsy: A bone marrow biopsy involves removing a sample of tissue from the bone marrow for examination under a microscope. This can help confirm the diagnosis of multiple myeloma and determine the extent of the disease.
6. Imaging tests: Imaging tests such as X-rays, CT scans, or MRI scans may be used to assess the extent of bone damage or other complications of multiple myeloma.
7. Genetic testing: Genetic testing may be used to identify specific genetic abnormalities that are associated with multiple myeloma and to monitor the response of the disease to treatment.

It's important to note that not all patients with MGUS or smoldering myeloma will develop multiple myeloma, and some patients with multiple myeloma may not have any symptoms at all. However, if you are experiencing any of the symptoms listed above or have a family history of multiple myeloma, it's important to talk to your doctor about your risk and any tests that may be appropriate for you.

There are several types of skin neoplasms, including:

1. Basal cell carcinoma (BCC): This is the most common type of skin cancer, and it usually appears as a small, fleshy bump or a flat, scaly patch. BCC is highly treatable, but if left untreated, it can grow and invade surrounding tissue.
2. Squamous cell carcinoma (SCC): This type of skin cancer is less common than BCC but more aggressive. It typically appears as a firm, flat, or raised bump on sun-exposed areas. SCC can spread to other parts of the body if left untreated.
3. Melanoma: This is the most serious type of skin cancer, accounting for only 1% of all skin neoplasms but responsible for the majority of skin cancer deaths. Melanoma can appear as a new or changing mole, and it's essential to recognize the ABCDE signs (Asymmetry, Border irregularity, Color variation, Diameter >6mm, Evolving size, shape, or color) to detect it early.
4. Sebaceous gland carcinoma: This rare type of skin cancer originates in the oil-producing glands of the skin and can appear as a firm, painless nodule on the forehead, nose, or other oily areas.
5. Merkel cell carcinoma: This is a rare and aggressive skin cancer that typically appears as a firm, shiny bump on the skin. It's more common in older adults and those with a history of sun exposure.
6. Cutaneous lymphoma: This type of cancer affects the immune system and can appear as a rash, nodules, or tumors on the skin.
7. Kaposi sarcoma: This is a rare type of skin cancer that affects people with weakened immune systems, such as those with HIV/AIDS. It typically appears as a flat, red or purple lesion on the skin.

While skin cancers are generally curable when detected early, it's important to be aware of your skin and notice any changes or unusual spots, especially if you have a history of sun exposure or other risk factors. If you suspect anything suspicious, see a dermatologist for an evaluation and potential biopsy. Remember, prevention is key to avoiding the harmful effects of UV radiation and reducing your risk of developing skin cancer.

There are several causes of hypergammaglobulinemia, including:

1. Chronic infections: Prolonged infections can cause an increase in the production of immunoglobulins to fight off the infection.
2. Autoimmune disorders: Conditions such as rheumatoid arthritis, lupus, and multiple sclerosis can cause the immune system to produce excessive amounts of antibodies.
3. Cancer: Some types of cancer, such as Hodgkin's disease and non-Hodgkin's lymphoma, can cause an increase in immunoglobulin production.
4. Genetic disorders: Certain genetic conditions, such as X-linked agammaglobulinemia, can lead to a deficiency or excess of immunoglobulins.
5. Medications: Certain medications, such as corticosteroids and chemotherapy drugs, can suppress the immune system and reduce the production of immunoglobulins.

Symptoms of hypergammaglobulinemia can include:

1. Infections: Recurring infections are a common symptom of hypergammaglobulinemia, as the excessive amount of antibodies can make it difficult for the body to fight off infections effectively.
2. Fatigue: Chronic infections and inflammation can cause fatigue and weakness.
3. Weight loss: Recurring infections and chronic inflammation can lead to weight loss and malnutrition.
4. Swollen lymph nodes: Enlarged lymph nodes are a common symptom of hypergammaglobulinemia, as the body tries to fight off infections.
5. Fever: Recurring fevers can be a symptom of hypergammaglobulinemia, as the body tries to fight off infections.
6. Night sweats: Excessive sweating at night can be a symptom of hypergammaglobulinemia.
7. Skin rashes: Certain types of skin rashes can be a symptom of hypergammaglobulinemia, such as a rash caused by allergic reactions to medications or infections.
8. Joint pain: Pain and stiffness in the joints can be a symptom of hypergammaglobulinemia, particularly if the excessive amount of antibodies is causing inflammation in the joints.
9. Headaches: Chronic headaches can be a symptom of hypergammaglobulinemia, particularly if the excessive amount of antibodies is causing inflammation in the brain or other parts of the body.
10. Swollen liver and spleen: Enlarged liver and spleen can be a symptom of hypergammaglobulinemia, as the body tries to filter out excess antibodies and fight off infections.

It is important to note that these symptoms can also be caused by other medical conditions, so it is essential to consult a healthcare professional for proper diagnosis and treatment. A healthcare professional may perform blood tests and other diagnostic procedures to determine the underlying cause of the symptoms and develop an appropriate treatment plan. Treatment for hypergammaglobulinemia typically involves addressing the underlying cause of the condition, such as infections, allergies, or autoimmune disorders, and may include medications to reduce inflammation and suppress the immune system.

There are several types of lymphoma, including:

1. Hodgkin lymphoma: This is a type of lymphoma that originates in the white blood cells called Reed-Sternberg cells. It is characterized by the presence of giant cells with multiple nucleoli.
2. Non-Hodgkin lymphoma (NHL): This is a type of lymphoma that does not meet the criteria for Hodgkin lymphoma. There are many subtypes of NHL, each with its own unique characteristics and behaviors.
3. Cutaneous lymphoma: This type of lymphoma affects the skin and can take several forms, including cutaneous B-cell lymphoma and cutaneous T-cell lymphoma.
4. Primary central nervous system (CNS) lymphoma: This is a rare type of lymphoma that develops in the brain or spinal cord.
5. Post-transplantation lymphoproliferative disorder (PTLD): This is a type of lymphoma that develops in people who have undergone an organ transplant, often as a result of immunosuppressive therapy.

The symptoms of lymphoma can vary depending on the type and location of the cancer. Some common symptoms include:

* Swollen lymph nodes
* Fever
* Fatigue
* Weight loss
* Night sweats
* Itching

Lymphoma is diagnosed through a combination of physical examination, imaging tests (such as CT scans or PET scans), and biopsies. Treatment options for lymphoma depend on the type and stage of the cancer, and may include chemotherapy, radiation therapy, immunotherapy, or stem cell transplantation.

Overall, lymphoma is a complex and diverse group of cancers that can affect people of all ages and backgrounds. While it can be challenging to diagnose and treat, advances in medical technology and research have improved the outlook for many patients with lymphoma.

The diagnosis of GVHD is based on a combination of clinical findings, laboratory tests, and biopsies. Treatment options include immunosuppressive drugs, corticosteroids, and in severe cases, stem cell transplantation reversal or donor lymphocyte infusion.

Prevention of GVHD includes selecting the right donor, using conditioning regimens that minimize damage to the recipient's bone marrow, and providing appropriate immunosuppression after transplantation. Early detection and management of GVHD are critical to prevent long-term complications and improve survival rates.

There are several subtypes of B-cell leukemia, including:

1. Chronic lymphocytic leukemia (CLL): This is the most common type of B-cell leukemia, and it typically affects older adults. CLL is a slow-growing cancer that can progress over time.
2. Acute lymphoblastic leukemia (ALL): This is a fast-growing and aggressive form of B-cell leukemia that can affect people of all ages. ALL is often treated with chemotherapy and sometimes with bone marrow transplantation.
3. Burkitt lymphoma: This is an aggressive form of B-cell leukemia that typically affects older adults in Africa and Asia. Burkitt lymphoma can be treated with chemotherapy and sometimes with bone marrow transplantation.
4. Hairy cell leukemia: This is a rare type of B-cell leukemia that is characterized by the presence of hair-like projections on the surface of cancer cells. Hairy cell leukemia can be treated with chemotherapy and sometimes with bone marrow transplantation.

The diagnosis of B-cell leukemia is based on a combination of physical examination, medical history, laboratory tests, and biopsies. Treatment options for B-cell leukemia include chemotherapy, bone marrow transplantation, and in some cases, targeted therapy with drugs that specifically target cancer cells. The prognosis for B-cell leukemia varies depending on the subtype of the disease and the patient's overall health.

Viremia is a condition where the virus is present in the bloodstream, outside of infected cells or tissues. This can occur during the acute phase of an infection, when the virus is actively replicating and spreading throughout the body. Viremia can also be seen in chronic infections, where the virus may persist in the blood for longer periods of time.

In some cases, viremia can lead to the development of antibodies against the virus, which can help to neutralize it and prevent its spread. However, if the viremia is not controlled, it can cause serious complications, such as sepsis or organ damage.

Diagnosis of viremia typically involves laboratory tests, such as PCR (polymerase chain reaction) or ELISA (enzyme-linked immunosorbent assay), which can detect the presence of virus in the blood. Treatment of viremia depends on the underlying cause and may include antiviral medications, supportive care, and management of any related complications.

There are several types of disease susceptibility, including:

1. Genetic predisposition: This refers to the inherent tendency of an individual to develop a particular disease due to their genetic makeup. For example, some families may have a higher risk of developing certain diseases such as cancer or heart disease due to inherited genetic mutations.
2. Environmental susceptibility: This refers to the increased risk of developing a disease due to exposure to environmental factors such as pollutants, toxins, or infectious agents. For example, someone who lives in an area with high levels of air pollution may be more susceptible to developing respiratory problems.
3. Lifestyle susceptibility: This refers to the increased risk of developing a disease due to unhealthy lifestyle choices such as smoking, lack of exercise, or poor diet. For example, someone who smokes and is overweight may be more susceptible to developing heart disease or lung cancer.
4. Immune system susceptibility: This refers to the increased risk of developing a disease due to an impaired immune system. For example, people with autoimmune disorders such as HIV/AIDS or rheumatoid arthritis may be more susceptible to opportunistic infections.

Understanding disease susceptibility can help healthcare providers identify individuals who are at risk of developing certain diseases and provide preventive measures or early intervention to reduce the risk of disease progression. Additionally, genetic testing can help identify individuals with a high risk of developing certain diseases, allowing for earlier diagnosis and treatment.

In summary, disease susceptibility refers to the predisposition of an individual to develop a particular disease or condition due to various factors such as genetics, environment, lifestyle choices, and immune system function. Understanding disease susceptibility can help healthcare providers identify individuals at risk and provide appropriate preventive measures or early intervention to reduce the risk of disease progression.

Dermatitis, contact can be acute or chronic, depending on the severity and duration of the exposure. In acute cases, the symptoms may resolve within a few days after removing the offending substance. Chronic dermatitis, on the other hand, can persist for weeks or even months, and may require ongoing treatment to manage the symptoms.

The symptoms of contact dermatitis can vary depending on the individual and the severity of the exposure. Common symptoms include:

* Redness and inflammation of the skin
* Itching and burning sensations
* Swelling and blistering
* Cracks or fissures in the skin
* Difficulty healing or recurring infections

In severe cases, contact dermatitis can lead to complications such as:

* Infection with bacteria or fungi
* Scarring and disfigurement
* Emotional distress and anxiety

Diagnosis of contact dermatitis is typically made based on the patient's medical history and physical examination. Allergic patch testing may also be performed to identify specific allergens that are causing the condition.

Treatment for contact dermatitis usually involves avoiding the offending substance and using topical or oral medications to manage symptoms. In severe cases, systemic corticosteroids or immunosuppressants may be prescribed. Phototherapy and alternative therapies such as herbal remedies or acupuncture may also be considered.

Prevention of contact dermatitis involves identifying and avoiding substances that cause an allergic reaction or skin irritation. Individuals with a history of contact dermatitis should take precautions when handling new substances, and should be aware of the potential for cross-reactivity between different allergens.

Examples of Immunologic Deficiency Syndromes include:

1. Primary Immunodeficiency Diseases (PIDDs): These are a group of genetic disorders that affect the immune system's ability to function properly. Examples include X-linked agammaglobulinemia, common variable immunodeficiency, and severe combined immunodeficiency.
2. Acquired Immunodeficiency Syndrome (AIDS): This is a condition that results from the human immunodeficiency virus (HIV) infection, which destroys CD4 cells, a type of immune cell that fights off infections.
3. Immune Thrombocytopenic Purpura (ITP): This is an autoimmune disorder that causes the immune system to attack and destroy platelets, which are blood cells that help the blood to clot.
4. Autoimmune Disorders: These are conditions in which the immune system mistakenly attacks and damages healthy cells and tissues in the body. Examples include rheumatoid arthritis, lupus, and multiple sclerosis.
5. Immunosuppressive Therapy-induced Immunodeficiency: This is a condition that occurs as a side effect of medications used to prevent rejection in organ transplant patients. These medications can suppress the immune system, increasing the risk of infections.

Symptoms of Immunologic Deficiency Syndromes can vary depending on the specific disorder and the severity of the immune system dysfunction. Common symptoms include recurrent infections, fatigue, fever, and swollen lymph nodes. Treatment options for these syndromes range from medications to suppress the immune system to surgery or bone marrow transplantation.

In summary, Immunologic Deficiency Syndromes are a group of disorders that result from dysfunction of the immune system, leading to recurrent infections and other symptoms. There are many different types of these syndromes, each with its own set of symptoms and treatment options.

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.

Pathologic neovascularization can be seen in a variety of conditions, including cancer, diabetic retinopathy, and age-related macular degeneration. In cancer, for example, the formation of new blood vessels can help the tumor grow and spread to other parts of the body. In diabetic retinopathy, the growth of new blood vessels in the retina can cause vision loss and other complications.

There are several different types of pathologic neovascularization, including:

* Angiosarcoma: a type of cancer that arises from the cells lining blood vessels
* Hemangiomas: benign tumors that are composed of blood vessels
* Cavernous malformations: abnormal collections of blood vessels in the brain or other parts of the body
* Pyogenic granulomas: inflammatory lesions that can form in response to trauma or infection.

The diagnosis of pathologic neovascularization is typically made through a combination of physical examination, imaging studies (such as ultrasound, CT scans, or MRI), and biopsy. Treatment options vary depending on the underlying cause of the condition, but may include medications, surgery, or radiation therapy.

In summary, pathologic neovascularization is a process that occurs in response to injury or disease, and it can lead to serious complications. It is important for healthcare professionals to be aware of this condition and its various forms in order to provide appropriate diagnosis and treatment.

Types of experimental neoplasms include:

* Xenografts: tumors that are transplanted into animals from another species, often humans.
* Transgenic tumors: tumors that are created by introducing cancer-causing genes into an animal's genome.
* Chemically-induced tumors: tumors that are caused by exposure to certain chemicals or drugs.

The use of experimental neoplasms in research has led to significant advances in our understanding of cancer biology and the development of new treatments for the disease. However, the use of animals in cancer research is a controversial topic and alternatives to animal models are being developed and implemented.

Also known as Burkitt's Lymphoma.

There are several types of lung neoplasms, including:

1. Adenocarcinoma: This is the most common type of lung cancer, accounting for approximately 40% of all lung cancers. It is a malignant tumor that originates in the glands of the respiratory tract and can be found in any part of the lung.
2. Squamous cell carcinoma: This type of lung cancer accounts for approximately 25% of all lung cancers and is more common in men than women. It is a malignant tumor that originates in the squamous cells lining the airways of the lungs.
3. Small cell lung cancer (SCLC): This is a highly aggressive form of lung cancer that accounts for approximately 15% of all lung cancers. It is often found in the central parts of the lungs and can spread quickly to other parts of the body.
4. Large cell carcinoma: This is a rare type of lung cancer that accounts for only about 5% of all lung cancers. It is a malignant tumor that originates in the large cells of the respiratory tract and can be found in any part of the lung.
5. Bronchioalveolar carcinoma (BAC): This is a rare type of lung cancer that originates in the cells lining the airways and alveoli of the lungs. It is more common in women than men and tends to affect older individuals.
6. Lymphangioleiomyomatosis (LAM): This is a rare, progressive, and often fatal lung disease that primarily affects women of childbearing age. It is characterized by the growth of smooth muscle-like cells in the lungs and can lead to cysts, lung collapse, and respiratory failure.
7. Hamartoma: This is a benign tumor that originates in the tissue of the lungs and is usually found in children. It is characterized by an overgrowth of normal lung tissue and can be treated with surgery.
8. Secondary lung cancer: This type of cancer occurs when cancer cells from another part of the body spread to the lungs through the bloodstream or lymphatic system. It is more common in people who have a history of smoking or exposure to other carcinogens.
9. Metastatic cancer: This type of cancer occurs when cancer cells from another part of the body spread to the lungs through the bloodstream or lymphatic system. It is more common in people who have a history of smoking or exposure to other carcinogens.
10. Mesothelioma: This is a rare and aggressive form of cancer that originates in the lining of the lungs or abdomen. It is caused by asbestos exposure and can be treated with surgery, chemotherapy, and radiation therapy.

Lung diseases can also be classified based on their cause, such as:

1. Infectious diseases: These are caused by bacteria, viruses, or other microorganisms and can include pneumonia, tuberculosis, and bronchitis.
2. Autoimmune diseases: These are caused by an overactive immune system and can include conditions such as sarcoidosis and idiopathic pulmonary fibrosis.
3. Genetic diseases: These are caused by inherited mutations in genes that affect the lungs and can include cystic fibrosis and primary ciliary dyskinesia.
4. Environmental diseases: These are caused by exposure to harmful substances such as tobacco smoke, air pollution, and asbestos.
5. Radiological diseases: These are caused by exposure to ionizing radiation and can include conditions such as radiographic breast cancer and lung cancer.
6. Vascular diseases: These are caused by problems with the blood vessels in the lungs and can include conditions such as pulmonary embolism and pulmonary hypertension.
7. Tumors: These can be benign or malignant and can include conditions such as lung metastases and lung cancer.
8. Trauma: This can include injuries to the chest or lungs caused by accidents or other forms of trauma.
9. Congenital diseases: These are present at birth and can include conditions such as bronchopulmonary foregut malformations and congenital cystic adenomatoid malformation.

Each type of lung disease has its own set of symptoms, diagnosis, and treatment options. It is important to seek medical attention if you experience any persistent or severe respiratory symptoms, as early diagnosis and treatment can improve outcomes and quality of life.

Crohn's disease can affect any part of the GI tract, from the mouth to the anus, and causes symptoms such as abdominal pain, diarrhea, fatigue, and weight loss. Ulcerative colitis primarily affects the colon and rectum and causes symptoms such as bloody stools, abdominal pain, and weight loss.

Both Crohn's disease and ulcerative colitis are chronic conditions, meaning they cannot be cured but can be managed with medication and lifestyle changes. Treatment options for IBD include anti-inflammatory medications, immunosuppressants, and biologics. In severe cases, surgery may be necessary to remove damaged portions of the GI tract.

There is no known cause of IBD, although genetics, environmental factors, and an abnormal immune response are thought to play a role. The condition can have a significant impact on quality of life, particularly if left untreated or poorly managed. Complications of IBD include malnutrition, osteoporosis, and increased risk of colon cancer.

Preventing and managing IBD requires a comprehensive approach that includes medication, dietary changes, stress management, and regular follow-up with a healthcare provider. With proper treatment and lifestyle modifications, many people with IBD are able to manage their symptoms and lead active, fulfilling lives.

Neoplastic metastasis can occur in any type of cancer but are more common in solid tumors such as carcinomas (breast, lung, colon). It is important for cancer diagnosis and prognosis because metastasis indicates that the cancer has spread beyond its original site and may be more difficult to treat.

Metastases can appear at any distant location but commonly found sites include the liver, lungs, bones, brain, and lymph nodes. The presence of metastases indicates a higher stage of cancer which is associated with lower survival rates compared to localized cancer.

CMV infections are more common in people with weakened immune systems, such as those with HIV/AIDS, cancer, or taking immunosuppressive drugs after an organ transplant. In these individuals, CMV can cause severe and life-threatening complications, such as pneumonia, retinitis (inflammation of the retina), and gastrointestinal disease.

In healthy individuals, CMV infections are usually mild and may not cause any symptoms at all. However, in some cases, CMV can cause a mononucleosis-like illness with fever, fatigue, and swollen lymph nodes.

CMV infections are diagnosed through a combination of physical examination, blood tests, and imaging studies such as CT scans or MRI. Treatment is generally not necessary for mild cases, but may include antiviral medications for more severe infections. Prevention strategies include avoiding close contact with individuals who have CMV, practicing good hygiene, and considering immunoprophylaxis (prevention of infection through the use of immune globulin) for high-risk individuals.

Overall, while CMV infections can be serious and life-threatening, they are relatively rare in healthy individuals and can often be treated effectively with supportive care and antiviral medications.

There are several different types of leukemia, including:

1. Acute Lymphoblastic Leukemia (ALL): This is the most common type of leukemia in children, but it can also occur in adults. It is characterized by an overproduction of immature white blood cells called lymphoblasts.
2. Acute Myeloid Leukemia (AML): This type of leukemia affects the bone marrow's ability to produce red blood cells, platelets, and other white blood cells. It can occur at any age but is most common in adults.
3. Chronic Lymphocytic Leukemia (CLL): This type of leukemia affects older adults and is characterized by the slow growth of abnormal white blood cells called lymphocytes.
4. Chronic Myeloid Leukemia (CML): This type of leukemia is caused by a genetic mutation in a gene called BCR-ABL. It can occur at any age but is most common in adults.
5. Hairy Cell Leukemia: This is a rare type of leukemia that affects older adults and is characterized by the presence of abnormal white blood cells called hairy cells.
6. Myelodysplastic Syndrome (MDS): This is a group of disorders that occur when the bone marrow is unable to produce healthy blood cells. It can lead to leukemia if left untreated.

Treatment for leukemia depends on the type and severity of the disease, but may include chemotherapy, radiation therapy, targeted therapy, or stem cell transplantation.

HIV seropositivity is typically diagnosed through a blood test called an enzyme-linked immunosorbent assay (ELISA). This test detects the presence of antibodies against HIV in the blood by using specific proteins on the surface of the virus. If the test is positive, it means that the individual has been infected with HIV.

HIV seropositivity is an important diagnostic criterion for AIDS (Acquired Immune Deficiency Syndrome), which is a condition that develops when the immune system is severely damaged by HIV infection. AIDS is diagnosed based on a combination of symptoms and laboratory tests, including HIV seropositivity.

HIV seropositivity can be either primary (acute) or chronic. Primary HIV seropositivity occurs when an individual is first infected with HIV and their immune system produces antibodies against the virus. Chronic HIV seropositivity occurs when an individual has been living with HIV for a long time and their immune system has produced antibodies that remain in their bloodstream.

HIV seropositivity can have significant implications for an individual's health and quality of life, as well as their social and economic well-being. It is important for individuals who are HIV seropositive to receive appropriate medical care and support to manage their condition and prevent the transmission of HIV to others.

There are several types of dermatitis, including:

1. Atopic dermatitis: a chronic condition characterized by dry, itchy skin and a tendency to develop allergies.
2. Contact dermatitis: a localized reaction to an allergen or irritant that comes into contact with the skin.
3. Seborrheic dermatitis: a condition characterized by redness, itching, and flaking skin on the scalp, face, or body.
4. Psoriasis: a chronic condition characterized by thick, scaly patches on the skin.
5. Cutaneous lupus erythematosus: a chronic autoimmune disorder that can cause skin rashes and lesions.
6. Dermatitis herpetiformis: a rare condition characterized by itchy blisters or rashes on the skin.

Dermatitis can be diagnosed through a physical examination, medical history, and sometimes laboratory tests such as patch testing or biopsy. Treatment options for dermatitis depend on the cause and severity of the condition, but may include topical creams or ointments, oral medications, phototherapy, or lifestyle changes such as avoiding allergens or irritants.

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.

There are several factors that can contribute to bone resorption, including:

1. Hormonal changes: Hormones such as parathyroid hormone (PTH) and calcitonin can regulate bone resorption. Imbalances in these hormones can lead to excessive bone resorption.
2. Aging: As we age, our bones undergo remodeling more frequently, leading to increased bone resorption.
3. Nutrient deficiencies: Deficiencies in calcium, vitamin D, and other nutrients can impair bone health and lead to excessive bone resorption.
4. Inflammation: Chronic inflammation can increase bone resorption, leading to bone loss and weakening.
5. Genetics: Some genetic disorders can affect bone metabolism and lead to abnormal bone resorption.
6. Medications: Certain medications, such as glucocorticoids and anticonvulsants, can increase bone resorption.
7. Diseases: Conditions such as osteoporosis, Paget's disease of bone, and bone cancer can lead to abnormal bone resorption.

Bone resorption can be diagnosed through a range of tests, including:

1. Bone mineral density (BMD) testing: This test measures the density of bone in specific areas of the body. Low BMD can indicate bone loss and excessive bone resorption.
2. X-rays and imaging studies: These tests can help identify abnormal bone growth or other signs of bone resorption.
3. Blood tests: Blood tests can measure levels of certain hormones and nutrients that are involved in bone metabolism.
4. Bone biopsy: A bone biopsy can provide a direct view of the bone tissue and help diagnose conditions such as Paget's disease or bone cancer.

Treatment for bone resorption depends on the underlying cause and may include:

1. Medications: Bisphosphonates, hormone therapy, and other medications can help slow or stop bone resorption.
2. Diet and exercise: A healthy diet rich in calcium and vitamin D, along with regular exercise, can help maintain strong bones.
3. Physical therapy: In some cases, physical therapy may be recommended to improve bone strength and mobility.
4. Surgery: In severe cases of bone resorption, surgery may be necessary to repair or replace damaged bone tissue.

Malignant prostatic neoplasms are cancerous tumors that can be aggressive and spread to other parts of the body (metastasize). The most common type of malignant prostatic neoplasm is adenocarcinoma of the prostate, which accounts for approximately 95% of all prostate cancers. Other types of malignant prostatic neoplasms include sarcomas and small cell carcinomas.

Prostatic neoplasms can be diagnosed through a variety of tests such as digital rectal examination (DRE), prostate-specific antigen (PSA) test, imaging studies (ultrasound, CT scan or MRI), and biopsy. Treatment options for prostatic neoplasms depend on the type, stage, and grade of the tumor, as well as the patient's age and overall health. Treatment options can include active surveillance, surgery (robotic-assisted laparoscopic prostatectomy or open prostatectomy), radiation therapy (external beam radiation therapy or brachytherapy), and hormone therapy.

In summary, Prostatic Neoplasms are tumors that occur in the prostate gland, which can be benign or malignant. The most common types of malignant prostatic neoplasms are adenocarcinoma of the prostate, and other types include sarcomas and small cell carcinomas. Diagnosis is done through a variety of tests, and treatment options depend on the type, stage, and grade of the tumor, as well as the patient's age and overall health.

1. Tumor size and location: Larger tumors that have spread to nearby tissues or organs are generally considered more invasive than smaller tumors that are confined to the original site.
2. Cellular growth patterns: The way in which cancer cells grow and divide can also contribute to the overall invasiveness of a neoplasm. For example, cells that grow in a disorganized or chaotic manner may be more likely to invade surrounding tissues.
3. Mitotic index: The mitotic index is a measure of how quickly the cancer cells are dividing. A higher mitotic index is generally associated with more aggressive and invasive cancers.
4. Necrosis: Necrosis, or the death of cells, can be an indication of the level of invasiveness of a neoplasm. The presence of significant necrosis in a tumor is often a sign that the cancer has invaded surrounding tissues and organs.
5. Lymphovascular invasion: Cancer cells that have invaded lymphatic vessels or blood vessels are considered more invasive than those that have not.
6. Perineural invasion: Cancer cells that have invaded nerve fibers are also considered more invasive.
7. Histological grade: The histological grade of a neoplasm is a measure of how abnormal the cancer cells look under a microscope. Higher-grade cancers are generally considered more aggressive and invasive than lower-grade cancers.
8. Immunohistochemical markers: Certain immunohistochemical markers, such as Ki-67, can be used to evaluate the proliferative activity of cancer cells. Higher levels of these markers are generally associated with more aggressive and invasive cancers.

Overall, the degree of neoplasm invasiveness is an important factor in determining the likelihood of the cancer spreading to other parts of the body (metastasizing) and in determining the appropriate treatment strategy for the patient.

Orthomyxoviridae infections are a group of viral infections caused by the Orthomyxoviridae family of viruses, which includes influenza A and B viruses, as well as other related viruses. These infections can affect both humans and animals and can cause a range of symptoms, from mild to severe.

The most common type of Orthomyxoviridae infection is seasonal influenza, which occurs when the virus is transmitted from person to person through the air or by contact with infected surfaces. Other types of Orthomyxoviridae infections include:

1. Pandemic influenza: This occurs when a new strain of the virus emerges and spreads quickly around the world, causing widespread illness and death. Examples of pandemic influenza include the Spanish flu of 1918 and the Asian flu of 1957.
2. Avian influenza: This occurs when birds are infected with the virus and can be transmitted to humans through close contact with infected birds or their droppings.
3. Swine influenza: This occurs when pigs are infected with the virus and can be transmitted to humans through close contact with infected pigs or their droppings.
4. H5N1 and H7N9: These are two specific types of bird flu viruses that have caused serious outbreaks in humans in recent years.

Symptoms of Orthomyxoviridae infections can include fever, cough, sore throat, runny nose, muscle aches, and fatigue. In severe cases, these infections can lead to pneumonia, bronchitis, and other respiratory complications, as well as hospitalization and even death.

Diagnosis of Orthomyxoviridae infections is typically made through a combination of physical examination, medical history, and laboratory tests, such as PCR (polymerase chain reaction) or viral culture. Treatment is generally focused on relieving symptoms and supporting the immune system, with antiviral medications may be used in severe cases.

Prevention of Orthomyxoviridae infections can include avoiding close contact with infected birds or pigs, wearing protective clothing and gear when handling animals, and practicing good hygiene such as washing hands frequently. Vaccines are also available for some species of birds and pigs to protect against these viruses.

Overall, Orthomyxoviridae is a family of viruses that can cause serious illness in humans and other animals, and it's important to take precautions to prevent exposure and spread of these viruses.

The symptoms of MS can vary widely depending on the location and severity of the damage to the CNS. Common symptoms include:

* Weakness, numbness, or tingling in the limbs
* Fatigue
* Vision problems, such as blurred vision, double vision, or loss of vision
* Difficulty with balance and coordination
* Tremors or spasticity
* Memory and concentration problems
* Mood changes, such as depression or mood swings
* Bladder and bowel problems

There is no cure for MS, but various treatments can help manage the symptoms and slow the progression of the disease. These treatments include:

* Disease-modifying therapies (DMTs) - These medications are designed to reduce the frequency and severity of relapses, and they can also slow the progression of disability. Examples of DMTs include interferons, glatiramer acetate, natalizumab, fingolimod, dimethyl fumarate, teriflunomide, and alemtuzumab.
* Steroids - Corticosteroids can help reduce inflammation during relapses, but they are not a long-term solution.
* Pain management medications - Pain relievers, such as acetaminophen or nonsteroidal anti-inflammatory drugs (NSAIDs), can help manage pain caused by MS.
* Muscle relaxants - These medications can help reduce spasticity and tremors.
* Physical therapy - Physical therapy can help improve mobility, balance, and strength.
* Occupational therapy - Occupational therapy can help with daily activities and assistive devices.
* Speech therapy - Speech therapy can help improve communication and swallowing difficulties.
* Psychological counseling - Counseling can help manage the emotional and psychological aspects of MS.

It's important to note that each person with MS is unique, and the best treatment plan will depend on the individual's specific symptoms, needs, and preferences. It's essential to work closely with a healthcare provider to find the most effective treatment plan.

The hallmark of HIGM1 is an excessive production of IgM antibodies, which are the largest and most complex antibodies produced by B cells. This results in an abnormally high level of IgM antibodies in the blood, often exceeding 100 times the normal upper limit. The excessive IgM production can lead to a variety of complications, including recurrent infections, autoimmune disorders, and cancer.

People with HIGM1 typically experience frequent and recurrent infections, particularly respiratory and gastrointestinal infections, and may also develop autoimmune disorders such as autoimmune hemolytic anemia or immune thrombocytopenia. Cancer, particularly lymphoma, is a significant risk for individuals with HIGM1.

There is currently no cure for HIGM1, and treatment is focused on managing the symptoms and preventing complications. This may include antibiotics to treat infections, immunoglobulin replacement therapy to boost the immune system, and medications to suppress the immune system and reduce the risk of autoimmune disorders. Stem cell transplantation has been attempted as a potential cure for HIGM1, but it is still an experimental treatment and its efficacy and safety have not been fully established.

HIGM1 is a rare disorder, and its prevalence is not well understood. However, it is believed to affect approximately 1 in 1 million people worldwide. The disorder is usually inherited in an autosomal recessive pattern, meaning that individuals must inherit two copies of the mutated gene, one from each parent, to develop the condition.

Overall, Hyper-IgM Immunodeficiency Syndrome, Type 1 (HIGM1) is a rare and complex disorder characterized by impaired immune function, increased risk of infections, and a range of other symptoms. While there is currently no cure for the condition, ongoing research and clinical trials are exploring new treatments and potential cures for HIGM1. With proper management and care, individuals with HIGM1 can lead fulfilling lives, but it is important for them to receive early and accurate diagnosis and ongoing medical attention to manage their symptoms and prevent complications.

There are several types of hypersensitivity reactions, including:

1. Type I hypersensitivity: This is also known as immediate hypersensitivity and occurs within minutes to hours after exposure to the allergen. It is characterized by the release of histamine and other chemical mediators from immune cells, leading to symptoms such as hives, itching, swelling, and difficulty breathing. Examples of Type I hypersensitivity reactions include allergies to pollen, dust mites, or certain foods.
2. Type II hypersensitivity: This is also known as cytotoxic hypersensitivity and occurs within days to weeks after exposure to the allergen. It is characterized by the immune system producing antibodies against specific proteins on the surface of cells, leading to their destruction. Examples of Type II hypersensitivity reactions include blood transfusion reactions and serum sickness.
3. Type III hypersensitivity: This is also known as immune complex hypersensitivity and occurs when antigens bind to immune complexes, leading to the formation of deposits in tissues. Examples of Type III hypersensitivity reactions include rheumatoid arthritis and systemic lupus erythematosus.
4. Type IV hypersensitivity: This is also known as delayed-type hypersensitivity and occurs within weeks to months after exposure to the allergen. It is characterized by the activation of T cells, leading to inflammation and tissue damage. Examples of Type IV hypersensitivity reactions include contact dermatitis and toxic epidermal necrolysis.

The diagnosis of hypersensitivity often involves a combination of medical history, physical examination, laboratory tests, and elimination diets or challenges. Treatment depends on the specific type of hypersensitivity reaction and may include avoidance of the allergen, medications such as antihistamines or corticosteroids, and immunomodulatory therapy.

Adenocarcinoma is a term used to describe a variety of different types of cancer that arise in glandular tissue, including:

1. Colorectal adenocarcinoma (cancer of the colon or rectum)
2. Breast adenocarcinoma (cancer of the breast)
3. Prostate adenocarcinoma (cancer of the prostate gland)
4. Pancreatic adenocarcinoma (cancer of the pancreas)
5. Lung adenocarcinoma (cancer of the lung)
6. Thyroid adenocarcinoma (cancer of the thyroid gland)
7. Skin adenocarcinoma (cancer of the skin)

The symptoms of adenocarcinoma depend on the location of the cancer and can include:

1. Blood in the stool or urine
2. Abdominal pain or discomfort
3. Changes in bowel habits
4. Unusual vaginal bleeding (in the case of endometrial adenocarcinoma)
5. A lump or thickening in the breast or elsewhere
6. Weight loss
7. Fatigue
8. Coughing up blood (in the case of lung adenocarcinoma)

The diagnosis of adenocarcinoma is typically made through a combination of imaging tests, such as CT scans, MRI scans, and PET scans, and a biopsy, which involves removing a sample of tissue from the affected area and examining it under a microscope for cancer cells.

Treatment options for adenocarcinoma depend on the location of the cancer and can include:

1. Surgery to remove the tumor
2. Chemotherapy, which involves using drugs to kill cancer cells
3. Radiation therapy, which involves using high-energy X-rays or other particles to kill cancer cells
4. Targeted therapy, which involves using drugs that target specific molecules on cancer cells to kill them
5. Immunotherapy, which involves using drugs that stimulate the immune system to fight cancer cells.

The prognosis for adenocarcinoma is generally good if the cancer is detected and treated early, but it can be more challenging to treat if the cancer has spread to other parts of the body.

Vaccinia is most commonly associated with smallpox, which is caused by a similar virus and was eradicated in the late 1970s through widespread vaccination. However, there have been occasional outbreaks of vaccinia in the United States and other countries since then, often linked to laboratory accidents or deliberate releases of the virus.

The treatment of vaccinia typically involves supportive care, such as rest, hydration, and antipyretic medications to reduce fever. Antiviral medications may also be used in some cases. Prevention of the disease relies on avoiding contact with infected animals or people, and on following proper infection control practices in laboratory and healthcare settings.

Vaccinia is a serious viral infection that can have severe consequences if left untreated. It is important to seek medical attention immediately if symptoms persist or worsen over time.

The symptoms of Arenaviridae infections can vary depending on the specific virus causing the infection, but they may include:

* Fever
* Headache
* Muscle pain
* Joint pain
* Sore throat
* Swollen lymph nodes
* Rash
* Seizures
* Meningitis
* Encephalitis (inflammation of the brain)

Some Arenaviridae infections can be transmitted to humans through contact with infected rodents or other animals, while others are spread by blood transfusions or organ transplantation. There is no specific treatment for Arenaviridae infections, and treatment is primarily focused on relieving symptoms and managing complications.

Examples of Arenaviridae infections include:

* Lymphocytic choriomeningitis (LCMV)
* Venezuelan equine encephalitis (VEE)
* Eastern equine encephalitis (EEE)
* Western equine encephalitis (WEE)
* Sabia virus infection

It's important to note that Arenaviridae infections can be severe and potentially life-threatening, so if you suspect you or someone else may have been infected, it's important to seek medical attention immediately.

The symptoms of lymphoma, T-cell, cutaneous can vary depending on the location and severity of the cancer, but may include:

* Red, scaly patches or lesions on the skin
* Itching, burning, or pain on the skin
* Swollen lymph nodes
* Fever
* Fatigue

Lymphoma, T-cell, cutaneous is a relatively rare type of cancer, and it can be difficult to diagnose. A doctor will typically perform a biopsy (removing a small sample of tissue from the affected area) to confirm the diagnosis. Treatment options may include:

* Topical medications (applied directly to the skin)
* Phototherapy (exposure to specific wavelengths of light)
* Chemotherapy (using drugs to kill cancer cells)
* Radiation therapy (using high-energy radiation to kill cancer cells)
* Targeted therapy (using drugs or other substances to target specific molecules on cancer cells)

Overall, the prognosis for lymphoma, T-cell, cutaneous is generally good, especially if the cancer is caught early and treated effectively. However, it can be a challenging condition to treat, and patients may experience significant discomfort and disfigurement.

These proteins are essential for white blood cells to stick together and migrate through the blood vessels into tissues, where they can fight off infections. The symptoms of Leukocyte Adhesion Deficiency syndrome vary depending on which gene is mutated and the severity of the mutation.

Some of the common symptoms include recurrent or persistent infections, poor wound healing, delayed development of the skin and mucous membranes, and difficulty fighting off certain types of bacteria, viruses, and fungi. The diagnosis of Leukocyte Adhesion Deficiency syndrome is based on a combination of clinical findings, laboratory tests that measure the function of white blood cells, and genetic analysis that identifies mutations in one of the genes involved in leukocyte adhesion.

Treatment for Leukocyte Adhesion Deficiency syndrome usually involves antibiotics to prevent or treat infections, topical creams or ointments to promote wound healing, and occasionally immunoglobulin replacement therapy to boost the immune system.

Several types of Leukocyte Adhesion Deficiency syndrome exist, each caused by a mutation in a different gene involved in leukocyte adhesion. The most common form of this disorder is called LAMA2 deficiency or Hereditary Angioedema with Giant Lymph Node.

Overall, early diagnosis and appropriate treatment can help manage symptoms and prevent complications associated with Leukocyte Adhesion Deficiency syndrome.

Leukocyte adhesion deficiency (LAD) is a group of rare genetic disorders characterized by impaired leukocyte trafficking and immune dysfunction. The disorders are caused by mutations in genes encoding proteins involved in leukocyte adhesion and migration, such as integrins and chemokine receptors.

There are several types of LAD, each with distinct clinical features and symptoms. The most common form of the disorder is LAMA2 deficiency, which affects approximately 1 in 50,000 individuals worldwide. Other forms of LAD include CD1a and CD1b deficiencies, which are less common but can have overlapping clinical features with LAMA2 deficiency.

The primary symptom of LAD is recurrent skin infections, particularly in childhood. Patients may also experience respiratory infections, gastrointestinal infections, and abscesses. In addition, some patients with LAD may develop chronic inflammation and fibrosis, which can lead to severe complications such as renal failure or blindness.

The diagnosis of LAD is based on a combination of clinical findings, laboratory tests, and genetic analysis. Laboratory tests may include flow cytometry, which can assess leukocyte function and adhesion properties, and molecular genetic testing, which can identify mutations in genes encoding integrins or other adhesion molecules.

Treatment of LAD typically involves antibiotics for recurrent skin and soft tissue infections, as well as management of any underlying chronic inflammation or fibrosis. In some cases, bone marrow transplantation may be considered as a curative therapy.

Overall, LAD is a rare and complex disorder that requires careful diagnosis and management by a multidisciplinary team of healthcare professionals. With appropriate treatment, many patients with LAD can lead active and productive lives, although some may experience ongoing complications or lifelong immune dysfunction.

The disease begins with endothelial dysfunction, which allows lipid accumulation in the artery wall. Macrophages take up oxidized lipids and become foam cells, which die and release their contents, including inflammatory cytokines, leading to further inflammation and recruitment of more immune cells.

The atherosclerotic plaque can rupture or ulcerate, leading to the formation of a thrombus that can occlude the blood vessel, causing ischemia or infarction of downstream tissues. This can lead to various cardiovascular diseases such as myocardial infarction (heart attack), stroke, and peripheral artery disease.

Atherosclerosis is a multifactorial disease that is influenced by genetic and environmental factors such as smoking, hypertension, diabetes, high cholesterol levels, and obesity. It is diagnosed by imaging techniques such as angiography, ultrasound, or computed tomography (CT) scans.

Treatment options for atherosclerosis include lifestyle modifications such as smoking cessation, dietary changes, and exercise, as well as medications such as statins, beta blockers, and angiotensin-converting enzyme (ACE) inhibitors. In severe cases, surgical interventions such as bypass surgery or angioplasty may be necessary.

In conclusion, atherosclerosis is a complex and multifactorial disease that affects the arteries and can lead to various cardiovascular diseases. Early detection and treatment can help prevent or slow down its progression, reducing the risk of complications and improving patient outcomes.

The symptoms of T-cell leukemia can vary depending on the severity of the disease, but they may include:

* Fatigue
* Weakness
* Frequent infections
* Easy bruising or bleeding
* Swollen lymph nodes
* Pain in the bones or joints
* Headaches
* Confusion or seizures (in severe cases)

T-cell leukemia is diagnosed through a combination of physical examination, blood tests, and bone marrow biopsy. Treatment typically involves chemotherapy and/or radiation therapy to kill cancer cells and restore the body's normal production of blood cells. In some cases, bone marrow transplantation may be recommended.

The prognosis for T-cell leukemia varies depending on the patient's age and overall health, as well as the aggressiveness of the disease. However, with current treatments, the 5-year survival rate is around 70% for children and adolescents, and around 40% for adults.

It's important to note that T-cell leukemia is relatively rare compared to other types of leukemia, such as acute myeloid leukemia (AML) or chronic lymphocytic leukemia (CLL). However, it can be a very aggressive and difficult-to-treat form of cancer, and patients with T-cell leukemia often require intensive treatment and close follow-up care.

These animal models allow researchers to study the underlying causes of arthritis, test new treatments and therapies, and evaluate their effectiveness in a controlled environment before moving to human clinical trials. Experimental arthritis models are used to investigate various aspects of the disease, including its pathophysiology, immunogenicity, and potential therapeutic targets.

Some common experimental arthritis models include:

1. Collagen-induced arthritis (CIA): This model is induced in mice by immunizing them with type II collagen, which leads to an autoimmune response and inflammation in the joints.
2. Rheumatoid arthritis (RA) models: These models are developed by transferring cells from RA patients into immunodeficient mice, which then develop arthritis-like symptoms.
3. Osteoarthritis (OA) models: These models are induced in animals by subjecting them to joint injury or overuse, which leads to degenerative changes in the joints and bone.
4. Psoriatic arthritis (PsA) models: These models are developed by inducing psoriasis in mice, which then develop arthritis-like symptoms.

Experimental arthritis models have contributed significantly to our understanding of the disease and have helped to identify potential therapeutic targets for the treatment of arthritis. However, it is important to note that these models are not perfect representations of human arthritis and should be used as tools to complement, rather than replace, human clinical trials.

Examples of delayed hypersensitivity reactions include contact dermatitis (a skin reaction to an allergic substance), tuberculin reactivity (a reaction to the bacteria that cause tuberculosis), and sarcoidosis (a condition characterized by inflammation in various organs, including the lungs and lymph nodes).

Delayed hypersensitivity reactions are important in the diagnosis and management of allergic disorders and other immune-related conditions. They can be detected through a variety of tests, including skin prick testing, patch testing, and blood tests. Treatment for delayed hypersensitivity reactions depends on the underlying cause and may involve medications such as antihistamines, corticosteroids, or immunosuppressants.

Herpesviridae infections are caused by the Herpesviridae family of viruses and can be transmitted through skin-to-skin contact, sexual contact, or from mother to child during pregnancy or childbirth. Symptoms of herpesviridae infections can vary depending on the type of virus and the individual infected, but may include fever, fatigue, muscle aches, and skin sores or rashes.

There is no cure for herpesviridae infections, but antiviral medications can help manage symptoms and reduce the risk of transmission to others. Good hygiene practices, such as washing hands regularly and avoiding close contact with those who are infected, can also help prevent the spread of these viruses.

Some common types of herpesviridae infections include:

* Herpes simplex virus (HSV) - Causes cold sores and genital herpes.
* Varicella-zoster virus (VZV) - Causes chickenpox and shingles.
* Human herpesvirus 8 (HHV-8) - Associated with certain types of cancer, such as Kaposi's sarcoma.

UC can be challenging to diagnose and treat, and there is no known cure. However, with proper management, it is possible for people with UC to experience long periods of remission and improve their quality of life. Treatment options include medications such as aminosalicylates, corticosteroids, and immunomodulators, as well as surgery in severe cases.

It's important for individuals with UC to work closely with their healthcare provider to develop a personalized treatment plan that takes into account their specific symptoms and needs. With the right treatment and support, many people with UC are able to manage their symptoms and lead active, fulfilling lives.

"CD40CD40 ligand." Journal of leukocyte biology 67.1 (2000): 2-17. Banchereau, Jacques, et al. "Immune and clinical responses ... "Long-term human B cell lines dependent on interleukin-4 and antibody to CD40." Science251.4989 (1991): 70-72. Banchereau, ...
van Kooten C, Banchereau J (January 2000). "CD40-CD40 ligand". Journal of Leukocyte Biology. 67 (1): 2-17. doi:10.1002/jlb.67.1 ... ISBN 978-0-8153-4093-5. Wang JH, Zhang YW, Zhang P, Deng BQ, Ding S, Wang ZK, Wu T, Wang J (September 2013). "CD40 ligand as a ... CD40 is also expressed on B cell precursors in the bone marrow, and there is some evidence that CD40-CD154 interactions may ... Human CD40 genome location and CD40 gene details page in the UCSC Genome Browser. PDBe-KB provides an overview of all the ...
May 1992). "Molecular and biological characterization of a murine ligand for CD40". Nature. 357 (6373): 80-82. Bibcode: ... Richard Armitage at Immunex cloned a cDNA encoding CD154 by screening an expression library with CD40-Ig. Randolph Noelle at ... Triggering PD-1 expressed on activated monocytes by its ligand PD-L1, induces IL-10 production which inhibits CD4 T-cell ... CD40 (protein) and CD40L) and through cytokines. Th cells are not a monolithic immunological entity because they are diverse in ...
van Kooten C, Banchereau J (January 2000). "CD40-CD40 ligand". Journal of Leukocyte Biology. 67 (1): 2-17. doi:10.1002/jlb.67.1 ... CD154, also called CD40 ligand or CD40L, is a protein that is primarily expressed on activated T cells and is a member of the ... Wang JH, Zhang YW, Zhang P, Deng BQ, Ding S, Wang ZK, Wu T, Wang J (September 2013). "CD40 ligand as a potential biomarker for ... "Entrez Gene: CD40LG CD40 ligand (TNF superfamily, member 5, hyper-IgM syndrome)". Lederman S, Yellin MJ, Krichevsky A, Belko J ...
... the signalling axis between the protein CD40 and its ligand, CD40L. Lutgens identified that the CD40 ligand was expressed in ... Lutgens focussed on the signalling pathways of CD40. She found that interactions between TRAF6 and CD40L were key drivers of ... She has developed lipid lowering compounds that can target the TRAF6 binding pocket for CD40. 2013 Netherlands Organisation for ...
This gene codes for the CD40 ligand, which is expressed on T cells. When the CD40 ligand binds CD40 on B cells, then the B cell ...
March 2001). "Regulation of CD40 and CD40 ligand by the AT-hook transcription factor AKNA". Nature. 410 (6826): 383-7. Bibcode: ... AKNA is known to upregulate expression of the receptor CD40 and its ligand CD40L/CD154. AKNA is an essential part in the ... December 2018). "The Human Papillomavirus (HPV) E6 Oncoprotein Regulates CD40 Expression via the AT-Hook Transcription Factor ...
February 2006). "Autoantibody to CD40 ligand in systemic lupus erythematosus: association with thrombocytopenia but not ...
Th1 cells activate macrophages by signaling with IFN-gamma and displaying the protein CD40 ligand. Other signals include TNF- ...
SAg activation in T-cells leads to production of CD40 ligand which activates isotype switching in B cells to IgG and IgM and ... Jabara HH, Geha RS (October 1996). "The superantigen toxic shock syndrome toxin-1 induces CD40 ligand expression and modulates ...
Dendritic cells secrete and respond to chemokines after stimulation to LPS, TNFα, or CD40 ligand. In maturing of DC production ... Chemokine (C-C motif) ligands 4 (also CCL4) previously known as macrophage inflammatory protein (MIP-1β), is a protein which in ...
Han S, Hathcock K... Kelsoe G (1995). Cellular interaction in germinal centers: Roles of CD40 ligand and B7-2 in established ...
CD40 is a co-stimulatory receptor on B cells that, when bound to CD40 ligand (CD40L), sends a signal to the B-cell receptor. ... Many CD40 Ligand Deficiency are first diagnosed after having PCP in their first year of life. The fungus is common and is ... "CD40 gene". Genetics Home Reference. Retrieved 27 November 2016. Lougaris V, Badolato R, Ferrari S, Plebani A (2005). "Hyper ... When there is a defect in CD40, this leads to defective T-cell interaction with B cells. Consequently, humoral immune response ...
2001). "Structure of CD40 ligand in complex with the Fab fragment of a neutralizing humanized antibody". Structure. 9 (4): 321- ...
2001). "Structure of CD40 ligand in complex with the Fab fragment of a neutralizing humanized antibody". Structure. 9 (4): 321- ...
"Immune responses to Pneumocystis murina are robust in healthy mice but largely absent in CD40 ligand-deficient mice". Journal ...
As assistant professor at Columbia, Lederman discovered the CD40-Ligand (CD154) and elucidated the molecular basis of T cell ... Dartmouth College challenged the CD40-Ligand patents, but the challenge (called an interference) was rejected on all claims. ... Lederman discovered the CD40-Ligand (CD154) and elucidated the molecular basis of T cell helper function. He also collaborated ... with Professor David Baltimore in identifying and functionally characterizing the CD40 signaling molecule, TRAF-3. Lederman's " ...
As mentioned above, CD40 is expressed on the surface of B cells, and its binding to CD40 ligand on activated T cells induces Ig ... The mutation in the TNFSF5 gene causes there to be no recognition of CD40 by CD40 ligand, and thus the T cells do not induce Ig ... Normally, CD40 ligand is expressed on activated T cells, and is necessary to induce immunoglobulin class switching from IgM to ... CD40 ligand is also required in the functional maturation of T lymphocytes and macrophages, so patients with this disorder have ...
1995). "HIV gp120 inhibits T cell activation by interfering with expression of costimulatory molecules CD40 ligand and CD80 ( ...
1995). "HIV gp120 inhibits T cell activation by interfering with expression of costimulatory molecules CD40 ligand and CD80 ( ...
1995). "HIV gp120 inhibits T cell activation by interfering with expression of costimulatory molecules CD40 ligand and CD80 ( ...
1995). "HIV gp120 inhibits T cell activation by interfering with expression of costimulatory molecules CD40 ligand and CD80 ( ...
"Signaling lymphocytic activation molecule is expressed on CD40 ligand-activated dendritic cells and directly augments ... Li SC, Gish G, Yang D, Coffey AJ, Forman-Kay JD, Ernberg I, Kay LE, Pawson T (2000). "Novel mode of ligand binding by the SH2 ...
1995). "HIV gp120 inhibits T cell activation by interfering with expression of costimulatory molecules CD40 ligand and CD80 ( ...
1995). "HIV gp120 inhibits T cell activation by interfering with expression of costimulatory molecules CD40 ligand and CD80 ( ...
Watanabe N, Hanabuchi S, Marloie-Provost MA, Antonenko S, Liu YJ, Soumelis V (June 2005). "Human TSLP promotes CD40 ligand- ... Liu YJ (August 2007). "Thymic stromal lymphopoietin and OX40 ligand pathway in the initiation of dendritic cell-mediated ...
Responses to human CD40 ligand/human interleukin-2 autologous cell vaccine in patients with B-cell chronic lymphocytic leukemia ...
In in vitro studies, it inhibited cell proliferation induced by CD40 ligands and induced cell lysis. Over three Phase 1 trials ... It is an antagonist to CD40 that was created by scientists at Chiron using Abgenix' XenoMouse transgenic mouse to generate ... Hassan SB, Sørensen JF, Olsen BN, Pedersen AE (April 2014). "Anti-CD40-mediated cancer immunotherapy: an update of recent and ... 627-II) A Fully Human Anti-CD40 Antagonistic Antibody, CHIR-12.12, Inhibit the Proliferation of Human B Cell Non-Hodgkin's ...
This gene codes for the CD40 ligand protein that binds the CD40 receptor and this binding activates an immune response. The ...
The transmembrane E3 ligase GRAIL ubiquitinates the costimulatory molecule CD40 ligand during the induction of T cell anergy". ...
However, it can also interact with other proteins (CLEC7A, CD137, CD40). For example, an interaction with CD40 on T-cells ... Galectin-9 is one of the most studied ligands for HAVCR2 (TIM-3) and is expressed on various tumor cells. ... Vaitaitis GM, Wagner DH (2012). "Galectin-9 controls CD40 signaling through a Tim-3 independent mechanism and redirects the ... "The Tim-3 ligand galectin-9 negatively regulates T helper type 1 immunity". Nature Immunology. 6 (12): 1245-52. doi:10.1038/ ...
... and includes several other non-cytokine ligands like receptors, CD40, CD27 and CD30, besides the ligands on which the family is ... Arimont A, Sun S, Smit MJ, Leurs R, de Esch IJ, de Graaf C (2017). "Structural Analysis of Chemokine Receptor-Ligand ...
CD40 deficiency, CD40 ligand deficiency, and Wiskott-Aldrich syndrome, but has been extended to secondary immunodeficiencies ...
1997). "In Vivo Microbial Stimulation Induces Rapid CD40 Ligand-independent Production of Interleukin 12 by Dendritic Cells and ... September 2003). "The Inducible CXCR3 Ligands Control Plasmacytoid Dendritic Cell Responsiveness to the Constitutive Chemokine ... and CD40 greatly enhancing their ability to activate T-cells. They also upregulate CCR7, a chemotactic receptor that induces ...
... ligand 5, and chemokine (C-X-C motif) ligand 10. These molecules activate both CD8+ T cells as well as natural killer cells. UV ... as well as costimulatory molecules CD40 and CD86. Experiments with animal models have shown that, even after UV inactivation, ... ligand 5, and chemokine (C-X-C motif) ligand 10. These molecules activate both CD8+ T cells as well as natural killer cells and ... Noguchi M, Sato N, Sugimori H, Mori K, Oshimi K (October 2001). "A minor E-selectin ligand, CD65, is critical for extravascular ...
CD40 is a costimulatory receptor on B cells that, when bound to CD40 ligand (CD40L), sends a signal to the B-cell receptor. ... When there is a defect in CD40, this leads to defective T-cell interaction with B cells. Consequently, humoral immune response ... "CD40 gene". Genetics Home Reference. Retrieved 27 November 2016. (Articles with short description, Short description is ... Hyper IgM syndromes is a group of primary immune deficiency disorders characterized by defective CD40 signaling; via B cells ...
If these receptors do not bind to their ligand, B cells do not receive the proper signals and cease to develop. Negative ... CD40L serves as a necessary co-stimulatory factor for B cell activation by binding the B cell surface receptor CD40, which ... such as pokeweed mitogen or anti-CD40 monoclonal antibodies, however, a study found a combination of R-848 and recombinant ...
... corresponding ligands, LAG-3 and CD40-L, respectively. A third class of receptors that can activate APCs are called toll-like ... Interest in the clinical use of TLR and CD40 agonistic antibodies in immuno-oncology wavered in the past decade. The APC ... APC Activators are agonists to APC surface-expressed ligands that, when bound, induce the maturation and activation of APCs. ... Professional APCs express MHC class II and CD40 molecules as surface receptors, and can be activated through direct ...
CD40 is a costimulatory receptor on B cells that, when bound to CD40 ligand (CD40L), sends a signal to the B-cell receptor. ... When there is a defect in CD40, this leads to defective T-cell interaction with B cells. Consequently, humoral immune response ... "CD40 gene". Genetics Home Reference. Retrieved 27 November 2016. (Articles with short description, Short description is ... Hyper IgM syndromes is a group of primary immune deficiency disorders characterized by defective CD40 signaling; via B cells ...
... expression correlates with rate of activation of B lymphocytes and it is under control of the B cell receptor, CD40, or ... It is not clear what ligands interact with CD83, but membrane-bound CD83 may homotypically interact with the soluble form, ... "Activated T cells induce rapid CD83 expression on B cells by engagement of CD40". Immunology Letters. 136 (2): 221-227. doi: ...
Ligand binding to the BCR also leads to the phosphorylation of the protein BCAP. This leads to the binding and activation of ... It has been shown that BCR signaling is synchronised with CD40 pathway activation provided by B-T cell interactions, and this ...
CD40 is a costimulatory receptor on B cells that, when bound to CD40 ligand (CD40L), sends a signal to the B-cell receptor. ... "CD40 gene". Genetics Home Reference. Retrieved 27 November 2016. (Use dmy dates from July 2013, Articles with short description ... When there is a defect in CD40, this leads to defective T-cell interaction with B cells. Consequently, humoral immune response ... Hyper IgM syndromes is a group of primary immune deficiency disorders characterized by defective CD40 signaling; via B cells ...
For instance, IKK2 is found to be mainly responsible for phosphorylating serine 536 in monocytes and macrophages, or in CD40 ... IKK1 functions as the major kinase phosphorylating serine 536 under different stimuli, such as the ligand activation of the ... 8-Tetrachlorodibenzo-p-dioxin suppresses tumor necrosis factor-alpha and anti-CD40-induced activation of NF-kappaB/Rel in ...
The structure of IL-24 has been found through crystallization by fusing a flexible linker with a ligand to its two receptors, ... After the combination of anti-IgM and CD40-L stimulation, B lymphocytes can also induce IL-24 expression. In response to immune ...
One reasonable way to consider lipid rafts is that small rafts can form concentrating platforms after ligand binding activation ... Their functions include signaling by BCR, modulation of that signaling by co-receptors, signaling by CD40, endocytosis of ... Lambert, Sylviane; Vind-Kezunovic, Dina; Karvinen, Susanna; Gniadecki, Robert (May 2006). "Ligand-Independent Activation of the ... "The Dipole Potential Modifies the Clustering and Ligand Binding Affinity of ErbB Proteins and Their Signaling Efficiency". Sci ...
... with CD28 and CD40 ligand on the T cell. Only licensed dendritic cells are able to activate cytotoxic T cells. T cell licensing ... When a T helper cell with a TCR specific for that peptide binds, the B cell marker CD40 binds to CD40L on the T cell surface. ... It also upregulates several co-stimulatory molecules required for T cell activation, including CD40 and B7. The latter can ... This occurs through the interaction of co-stimulatory molecules including B7 and CD40 on the dendritic cell, ...
... also known as CD40 ligand Tripartite ATP-independent periplasmic transporter, in prokaryotes trp RNA-binding attenuation ...
Noteworthy is the production of interleukin 2 (IL-2) as well as ɑ-chain of CD25 (which is a receptor of IL-2), CD40 ligand, ... Another ligand of CD80 is programmed death-ligand 1 (PD‐L1), expressed on the surface of T-cells, B-cells, DCs, and macrophages ... These two ligands are structurally homologous, and they compete with each other for binding sites. However, the bond with CTLA- ... CD80 is the ligand for the proteins CD28 (for autoregulation and intercellular association) and CTLA-4 (for attenuation of ...
This gene product protein, LMP1, mimics activated human TNF receptors (e.g. CD40, CD40, and RANK) in continuously stimulating ... PD-L1 (programmed death-ligand 1) functions to suppress the proliferation of antigen-specific T cells and promote the survival ...
Furthermore, type I NKT cells upregulate the costimulatory receptor CD154 (CD40 ligand), which, in conjunction with their ...
The protein encoded by this gene is a member of the tumor necrosis factor ligand (TNF) ligand family. This protein is a ligand ... Litinskiy MB, Nardelli B, Hilbert DM, He B, Schaffer A, Casali P, Cerutti A (September 2002). "DCs induce CD40-independent ... A proliferation-inducing ligand (APRIL), also known as tumor necrosis factor ligand superfamily member 13 (TNFSF13), is a ... Kelly K, Manos E, Jensen G, Nadauld L, Jones DA (February 2000). "APRIL/TRDL-1, a tumor necrosis factor-like ligand, stimulates ...
The costimulatory signal necessary to continue the immune response can come from B7-CD28 and CD40-CD40L interactions. When CD40 ... In the TNF family of molecules, the protein 4-1BB (CD137) on the T cell may bind to 4-1BB ligand (4-1BBL) on the APC. The B7 ( ...
View Human CD40 Ligand/TNFSF5 Antibody (AF617) datasheet. ... CD40 antigen ligand; CD40 Ligand; CD40L; CD40-L; CD40LG; ... Background: CD40 Ligand/TNFSF5. CD40 ligand, CD40L (also known as CD154, TRAP or gp39), is a 261 amino acid type II ... Reviews for Human CD40 Ligand/TNFSF5 Antibody. There are currently no reviews for this product. Be the first to review Human ... Detection of Human CD40 Ligand/TNFSF5 by Western Blot. Western blot shows lysates of Jurkat human acute T cell leukemia cells, ...
Platelet-CD40ligand interaction with melanoma cell and monocyte CD40 enhances ‎cellular procoagulant activity. Blood Coagul ... Widespread expression of CD40 in humans implies that its ligand has an important role in cancer pathogenesis (16): inhibiting ... Elevated serum soluble CD40 ligand in cancer patients may play an immunosuppressive role. Blood. 2012 Oct 11;120(15):3030-8. ... CD40 ligand on activated platelets triggers an inflammatory reaction of endothelial cells. Nature. 1998 Feb 5;391(6667):591-4. ...
keywords = "CD40 ligand, Platelet, Shear stress, Von Willebrand factor",. author = "Noriko Tamura and Minako Yoshida and Noriko ... We focused on the surface translocation of CD40 ligand (CD40L) molecules when the platelets are exposed to a high shear stress ... We focused on the surface translocation of CD40 ligand (CD40L) molecules when the platelets are exposed to a high shear stress ... We focused on the surface translocation of CD40 ligand (CD40L) molecules when the platelets are exposed to a high shear stress ...
Copy For Citation YİĞİT Y., ERSUNAN G., BİLİR Ö., KALKAN A., YAVAŞİ Ö., KAYAYURT K. 1st Intercontinental Emergency Medicine Congress, Antalya, Turkey, 15 - 18 May 2014 ...
A) Tumor necrosis factor-α (TNF-α); B) Interleukin-6 (IL-6); C) Interferon-γ (IFN-γ); D) Soluble CD40 ligand (sCD40L); E) IL-10 ...
EDIII fused with CD40 ligand. Horses: ↑IgG and neutralizing Ab titers. ND. No. [126]. ... A recombinant fusion protein consisting of West Nile virus envelope domain III fused in-frame with equine CD40 ligand induces ...
CD40LG: CD40 ligand. *CDAN1: codanin 1. *CDC6: cell division cycle 6. *CDC73: cell division cycle 73 ...
"Soluble CD40 ligand accumulates in stored blood components, primes neutrophils through CD40, and is a potential cofactor in the ... "Soluble CD40 ligand accumulates in stored blood components, primes neutrophils through CD40 and is a cofactor in the ... "Developmental changes in soluble CD40 ligand." The Journal of pediatrics.. 2008 Jan; 152(1):50-4, 54.e1. Epub 2007 Oct 24. ... "The platelet as an immune cell-CD40 ligand and transfusion immunomodulation." Immunologic research.. 2009 Dec; 45(2-3):251-60. ...
LIGANTE A CD40. CD40 LIGAND. LIGANDO CD40. LIVROS DE TEXTO [TIPO DE PUBLICAÇÃO]. TEXTBOOKS [PUBLICATION TYPE]. LIBROS DE TEXTO ...
The mechanisms regulating CD40 ligand gene expression are largely unknown. Optimal expression of CD40 ligand required ... indicating that calcineurin plays a key role in CD40 ligand gene expression. Cyclosporin A inhibited IL-4-driven CD40 ligand- ... CD40 ligand expression was inhibited by pretreatment of T cells with cyclosporin A. Cyclosporin A analogues inhibited CD40 ... The ligand for CD40 is expressed on activated T lymphocytes and delivers contact-dependent activation signals to B lymphocytes ...
CD30 Ligand [‎1]‎. CD4 Lymphocyte Count [‎9]‎. CD40 Ligand [‎1]‎. Cefoxitin [‎1]‎. ...
Additionally, CD40 is important for T cell-B cell interactions. The ligand of CD40 is CD154 (CD40 ligand). The 5C3 antibody has ... Ligand/Receptor CD154 (CD40 ligand) Cell Type B cells, Dendritic cells, Endothelial cells, Fibroblasts, Macrophages Biology ... CD40 is a 48 kD type I glycoprotein also known as BP50. It is a member of the TNFR superfamily primarily expressed on B cells, ... CD40 has been reported to be involved in B cell differentiation, costimulation, isotype class-switching, and protection of B ...
CD40 ligand inhibits Fas/CD95-mediated apoptosis of human blood-derived dendritic cells. Eur J Immunol. 1997 Dec. 27(12):3161-5 ... A central role of CD40 ligand in the regulation of CD4+ T-cell responses. Immunol Today. 1996 Sep. 17(9):410-4. [QxMD MEDLINE ... Ligation of CD40 on dendritic cells triggers the production of large amounts of IL-12, which enhances T-cell stimulatory ... These cells, rich in MHC classes I and II, have abundant molecules for T-cell binding and co-stimulation, which involves CD40, ...
OK432-activated human dendritic cells kill tumor cells via CD40/CD40 ligand interactions. Hill KS, Errington F, Steele LP, ...
Haematopoietic Stem Cell Transplantation for CD40 Ligand Deficiency: Results from an EBMT/ESID Inborn Error Working Party Study ... Haematopoietic stem cell transplantation for CD40 ligand deficiency: results from an EBMT Inborn Errors Working Party (IEWP) ...
... cluster of differentiation 41-ligand present on Th cell, bind to CD40 to activate APC; TCR: T cell receptor; BCR: B cell ... ligand-5/RANTES/its chemotactic for neutrophils; CCL2: chemokine [c-c-motif] ligand-2/MCP1; CCL3: chemokine [c-c-motif] ligand- ... F. Vu, U. Dianzani, C. F. Ware, T. Mak, and J. L. Gommerman, "ICOS, CD40, and lymphotoxin β receptors signal sequentially and ... CD40: cluster of differentiation 40/co-stimulatory protein present on antigen-presenting cell (APC); CD40L: ...
The companys lead compound in development is tegoprubart, an anti-CD40L antibody with high affinity for CD40 Ligand, a well- ... Eledon Pharmaceuticals is a clinical stage biotechnology company using its expertise in targeting the CD40 Ligand (CD40L, also ...
Lee, S. P., Ataga, K. I., Orringer, E. P., Phillips, D. R. & Parise, L. V. (2006) Biologically active CD40 ligand is elevated ... Lee et al., "Biologically active CD40 ligand is elevated in sickle cell anemia: potential role for platelet-mediated ... such as soluble CD40 ligand (sCD40L) (Lee, et al 2006), PF-4 (Westwick, et al 1983) and IL-1β (Wun, et al 2002). In healthy ... selectin P ligand (SELPLG), vitronectin receptor (VTNR) and ICAM-1 (van Gils, et al 2009). SCD platelets have been demonstrated ...
BACKGROUND: CD40 ligand(CD40L) is implicated in atherosclerotic plaque formation. OBJECTIVES: We investigated prospective ... Prospective study of circulating soluble CD40 ligand concentrations and the incidence of cardiovascular disease in a nested ... Ligante de CD40/sangue , Mediadores da Inflamação/sangue , Infarto do Miocárdio/epidemiologia , Acidente Vascular Cerebral/ ...
LIGANTE A CD40. CD40 LIGAND. LIGANDO CD40. LIVROS DE TEXTO [TIPO DE PUBLICAÇÃO]. TEXTBOOKS [PUBLICATION TYPE]. LIBROS DE TEXTO ...
Antigens, CD40. A member of the tumor necrosis factor receptor superfamily with specificity for CD40 LIGAND. It is found on ... CD40 Ligand. A membrane glycoprotein and differentiation antigen expressed on the surface of T-cells that binds to CD40 ... CD40CD40 LigandAntigens, CD20Antigens, ViralAntigens, CD28Antigens, CD44Antigens, CD7Antigens, CD14Antigens, CD2CD4-CD8 Ratio ... CD40CD40 LigandAntigens, CD20Antigens, ViralAntigens, CD28Antigens, CD44Antigens, CD7Antigens, CD14Antigens, CD2Antigens, CD5 ...
CD40 ligand. CD40LG. P29965. 1 Reference(s). T94S85. Collagen alpha-1(I) chain. COL1A1. P02452. 1 Reference(s). ...
Wuhan institute of Biotechnology B7, Biolake No.666 Gaoxin Road, Wuhan, Hubei, China. ...
CD40 CD40 Ligand CD40L CD44 CIC C1q CIC C3d Club Cell Protein Cluster of Differentiation 14 Clusterin Connective Tissue Growth ... Fas Ligand Ferritin Fetuin-A Fibrinogen-Like Protein 1 Fibroblast Growth Factor 19 Fibroblast Growth Factor 21 Fibronectin FSH ...
"A subset of human monocyte-derived dendritic cells expresses high levels of interleukin-12 in response to combined CD40 ligand ... "Flt3-ligand as a vaccine adjuvant: Results in a study of Flt3-ligand plus tetanus toxoid immunization." Journal of Applied ... "Multiple signals are required for maturation of human dendritic cells mobilized in vivo with Flt3 ligand." J Leukoc Biol 72, no ... "Multiple signals are required for IL-12 production by Flt-3 ligand mobilized dendritic cells." In Blood, 96:295A-295A. AMER SOC ...
Antoniades C, Bakogiannis C, Tousoulis D, et al., The CD40/CD40 ligand system. Linking inflammation with atherothrombosis, J Am ... Lee SP, Ataga KI, Orringer EP, et al., Biologically active CD40 ligand is elevated in sickle cell anemia: potential role for ... The sCD40L-CD40 interaction in this context promotes monocyte adhesion to vascular endothelium, endothelial activation and ... Danese S, de la Motte C, Sturm A, et al., Platelets trigger a CD40-dependent inflammatory response in the microvasculature of ...
  • CD40 ligand, CD40L (also known as CD154, TRAP or gp39), is a 261 amino acid type II transmembrane glycoprotein belonging to the TNF family, CD40L is expressed predominantly on activated CD4 + T lymphocytes, and also found in other types of cells, like NK cells, mast cells, basophils and eosinophils. (rndsystems.com)
  • The receptor of CD40L is CD40, a type I transmembrane glycoprotein belonging to the TNF receptor family. (rndsystems.com)
  • Although all monomeric, dimeric and trimeric forms of soluble CD40L can bind to CD40, the trimeric form of soluble CD40L has the most potent biological activity through oligomerization of cell surface CD40, a common feature of TNF receptor family members. (rndsystems.com)
  • We focused on the surface translocation of CD40 ligand (CD40L) molecules when the platelets are exposed to a high shear stress. (elsevier.com)
  • We have shown that interaction of CD40 with CD40L enables microglial activation in response to amyloid-beta peptide (Abeta), which is associated with Alzheimer's disease (AD)-like neuronal tau hyperphosphorylation in vivo. (nih.gov)
  • Conversely, in neuroblastoma cells overexpressing wild-type human APP, the CD40-CD40L interaction resulted in amyloidogenic APP processing. (nih.gov)
  • These findings suggest several possible mechanisms underlying mitigation of AD pathology in response to CD40L depletion and validate the CD40-CD40L interaction as a target for therapeutic intervention in AD. (nih.gov)
  • CD40 ligand (CD40L, also known as CD154) is an important costimulatory molecule found on the T-cell and is critical for the development of immunity. (nih.gov)
  • The 5C3 antibody has been reported to promote B cell proliferation in the presence of anti-IgM, IL-4 or PMA, partially blocking CD40 binding to CD40L, and B cells rescue from apoptosis. (biolegend.com)
  • Additional reported applications (for the relevant formats) include: costimulation of B cell proliferation 1 , partial inhibition of CD40 binding to CD40L 3 , and B cell rescue from apoptosis 1 . (biolegend.com)
  • 18. In situ expression of CD40, CD40L (CD154), IL-12, TNF-alpha, IFN-gamma and TGF-beta1 in murine lungs during slowly progressive primary tuberculosis. (nih.gov)
  • 20. CD40L induces proliferation, self-renewal, rescue from apoptosis, and production of cytokines by CD40-expressing AML blasts. (nih.gov)
  • Eledon Pharmaceuticals is a clinical stage biotechnology company using its expertise in targeting the CD40 Ligand (CD40L, also called CD154) pathway to develop potential treatments for persons requiring an organ or cell-based transplant, living with autoimmune disease, or living with ALS. (itbusinessnet.com)
  • The company's lead compound in development is tegoprubart, an anti-CD40L antibody with high affinity for CD40 Ligand, a well-validated biological target with broad therapeutic potential. (itbusinessnet.com)
  • RÉSUMÉ L'objectif de l'étude était d'évaler l'importance clinique du ligand de CD40 soluble (sCD40L) chez des patients atteints d'un carcinome hépatocellulaire (CHC) associé au virus de l'hépatite C (VHC). (who.int)
  • Prognostic effect of soluble CD40 ligand. (erdogan.edu.tr)
  • Expression of CD40 Ligand on T Cells and Soluble CD40 Ligand in Children With Kawasaki Disease: A Single-Center Preliminary Study From North India. (nih.gov)
  • Although LPS-stimulated DCs do lose their responsiveness to LPS about 24 hours after stimulation, they nevertheless remain perfectly capable of making inflammatory cytokines in response to signals from activated T cells, and to a combination of CD40-ligand plus soluble T-cell derived signals. (nih.gov)
  • The addition of recombinant human soluble CD40 IgG fusion protein (rsCD40-Ig) inhibited induction of IgE synthesis by rDiAg with IL-4. (fujita-hu.ac.jp)
  • PVDF membrane was probed with 1 µg/mL of Goat Anti-Human CD40 Ligand/TNFSF5 Antigen Affinity-purified Polyclonal Antibody (Catalog # AF617) followed by HRP-conjugated Anti-Goat IgG Secondary Antibody (Catalog # HAF017 ). (rndsystems.com)
  • 17. TLR9 Ligand (CpG Oligodeoxynucleotide) Induces CLL B-Cells to Differentiate into CD20(+) Antibody-Secreting Cells. (nih.gov)
  • CDC researchers have developed methods and adjuvants for enhancing a subject's immune response to respiratory syncytial virus (RSV) by inclusion of a CD40 binding protein. (nih.gov)
  • In direct ELISAs, approximately 20% cross-reactivity with recombinant mouse CD40 Ligand is observed and less than 1% cross-reactivity with recombinant human (rh) CD27 Ligand and rhCD30 Ligand is observed. (rndsystems.com)
  • Les concentrations sériques de sCD40L circulant et d'interleukine 10 circulante ont été analysées à l'aide de la méthode immuno-enzymatique chez 30 patients positifs pour le VHC avec un CHC, chez 30 patients patients positifs pour le VHC avec une cirrhose du foie, et chez 30 volontaires d'âge correspondant en bonne santé avec des anticorps anti-VHC négatifs servant de groupe témoin. (who.int)
  • A member of the tumor necrosis factor receptor superfamily with specificity for CD40 LIGAND. (lookformedical.com)
  • A membrane glycoprotein and differentiation antigen expressed on the surface of T-cells that binds to CD40 ANTIGENS on B-LYMPHOCYTES and induces their proliferation. (nih.gov)
  • CD40 is expressed on B lymphocytes, monocytes, dendritic cells and thymic epithelium. (rndsystems.com)
  • 5. CD40 ligation induces Apo-1/Fas expression on human B lymphocytes and facilitates apoptosis through the Apo-1/Fas pathway. (nih.gov)
  • 4. A phase I study of an adenoviral vector delivering a muc1 /CD40-ligand fusion protein in patients with advanced adenocarcinoma. (nih.gov)
  • CD40 has been reported to be involved in B cell differentiation, costimulation, isotype class-switching, and protection of B cells from apoptosis. (biolegend.com)
  • 4. Responsiveness of chronic lymphocytic leukemia B cells activated via surface Igs or CD40 to B-cell tropic factors. (nih.gov)
  • 8. Ligation of CD40 potentiates Fas-mediated activation of the cysteine protease CPP32, cleavage of its death substrate PARP, and apoptosis in Ramos-Burkitt lymphoma B cells. (nih.gov)
  • Evidence suggests that CD40-dependent activation of B-cells is important for generation of memory B-cells within the germinal centers. (lookformedical.com)
  • Moreover, in CD40-deficient mice, IgE production and MLN-B cell proliferation by rDiAg were completely absent. (fujita-hu.ac.jp)
  • CD40 is a 48 kD type I glycoprotein also known as BP50. (biolegend.com)
  • 15. CD40 ligand exerts differential effects on the expression of I gamma transcripts in subclones of an IgM+ human B cell lymphoma line. (nih.gov)
  • Detects human CD40 Ligand/TNFSF5 in direct ELISAs and Western blots. (rndsystems.com)
  • Detection of Human CD40 Ligand/TNFSF5 by Western Blot. (rndsystems.com)
  • 6. A dual role for both CD40-ligand and TNF-alpha in controlling human B cell death. (nih.gov)
  • CD40 ligand, a proinflamatory and atherogenic cytokine, and CRP were also reported to be elevated in type 1 diabetic patients. (nih.gov)
  • Targeting signal 1 through CD45RB synergizes with CD40 ligand blockade and promotes long term engraftment and tolerance in stringent transplant models. (umassmed.edu)
  • Additionally, CD40 is important for T cell-B cell interactions. (biolegend.com)
  • Expression of CD40 Ligand on T Cells and Soluble CD40 Ligand in Children With Kawasaki Disease: A Single-Center Preliminary Study From North India. (nih.gov)
  • CD40 ligand, a proinflamatory and atherogenic cytokine, and CRP were also reported to be elevated in type 1 diabetic patients. (nih.gov)
  • Despite the fact that the hyper-IgM syndrome mutations are dispersed in the primary sequence, a large fraction of them are clustered in space in the vicinity of a surface loop, close to the predicted CD40-binding site. (nih.gov)