self-antigen


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self-antigen

 [self-an´tĭ-jen]
any constituent of the body's own tissues capable of stimulating autoimmunity. See also immunity.

self-antigen

/self-an·ti·gen/ (self-an´tĭ-jen) autoantigen.

self-antigen

autoantibody

Any antibody produced by an organism against one of its own—self-antigens.

Autoantibodies
Examples of autoantibodies and disease associations
• Anti-actin antibodies—coeliac disease.
• Anti-centromere antibodies—CREST syndrome.
• Anti-ganglioside antibodies—acute motor neuronal neuropathy.
• Antimitochondrial antibody—primary biliary cirrhosis.
• Anti-neutrophil cytoplasmic antibody—Wegener’s granulomatosis (in neutrophil cytoplasm).
• Anti-neutrophil cytoplasmic antibody—Churg-Strauss syndrome, microscopic polyangiitis, systemic vasculitides (perinuclear location).
• Anti-nuclear antibodies (e.g., anti-SSA/Ro)—systemic lupus erythematosus.
• Anti-signal recognition peptide—polymyositis.
• Anti-smooth muscle antibody—chronic autoimmune hepatitis.
• Anti-glomerular basement membrane antibodies.
• Anti-parietal cell antibodies, and others.
• Anti-nuclear antibodies (ANA).
• Anti-smooth muscle actin (SMA).
• Anti-liver-kidney-microsomal antibody (LKM), 2 types:
   - Anti-mitochondrial (AMA);
   - Perinuclear antineutrophil cytoplasmic (pANCA).
• Anti-soluble liver antigen (SLA), other autoantibodies.
• ANA and SMAs are known to be positive in AIH, PBC, PSC, HCV, HBV, HDV, NASH, drug-induced hepatitis.

self-antigen

any constituent of the body's own tissues capable of stimulating autoimmunity. See also immunity.
References in periodicals archive ?
11,12) This result suggested that immune responses to RNA but not DNA are crucial in the development of lupus though it is not yet clear why RNA-related self-antigens but not DNA ones are pathogenic.
During mechanical injury, self-antigens and cytokines are released without consistently stimulating pathogen-specific responses.
Characterized by reduced levels of circulating red blood cells resulting from their destruction by antibodies binding to self-antigens on the surface of the red blood cell.
Association of these antibodies to self-antigens and complement factors will form circulating ICs which are likely one of the source materials for autoreactive B cell activation in SLE.
Medullary thymic epithelial cells (mTECs) are critical in this process because they express a diverse repertoire of peripheral tissue-restricted self-antigens (TRAs).
Whereas antibodies against pathogen-associated antigens provide defense against infection, autoantibodies target a wide variety of cell surface, cytoplasmic, and nuclear self-antigens.
Cellular and humoral immune reaction against a variety of neural cell antigens, such as myelin basic protein, myelin oligodendrocyte glycoprotein, myelin associated glycoprotein, ganglioside, sulfatide, and many other self-antigens, may result in a neuroimmune disorder including interference with neurotransmission.
The researchers review posttranslational modifications of self-antigens, histo-blood group antigens as autoantigens, differential regulation of the IL-10 gene in Th1 and Th2 T cells, long-lived plasma cells, and a new automated fluorescence PR3 and MPO-ANCA immunoassay.
Alterations of the fetal immune environment might pre-program the highly sensitive fetal immune system for aberrant immune regulation, leading to a loss of tolerance to self-antigens and resulting in an increased risk for autoimmune disease.
A sampling of topics: the anatomy of mucosal immune responses, uptake of antigens from the intestine by dendritic cell function, natural killer T cells in mucosal homeostasis, regulation of autoreactive T cell function by oral tolerance to self-antigens, oral insulin therapy to prevent progression of immune-mediated (type 1) diabetes, and intestinal myofibroblasts and immune tolerance.
Alterations of the fetal immune environment might preprogram the highly sensitive fetal immune system for aberrant immune regulation, leading to a loss of tolerance to self-antigens and resulting in an increased risk for autoimmune disease.
We define self-antigens as those either encoded by germ-line sequences or caused by recombinational events attributable to exposure to environmental biohazardous entities (3).