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 ?
During mechanical injury, self-antigens and cytokines are released without consistently stimulating pathogen-specific responses.
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).
The ability of sCD83-treated dendritic cells to induce regulatory T cells, which are responsible for suppressing the immune response and maintaining tolerance to self-antigens, provides potential mechanistic insight into its promising tolerogenic properties and further reinforces our commitment to move this exciting protein into a clinical setting," commented Charles Nicolette, Ph.
Novel Approach May Have Potential to Revolutionize Treatment of Certain Autoimmune Diseases By Selectively Neutralizing Destructive Self-Antigens While Leaving Rest of Immune System Unaffected--
Possible mechanisms for environmentally induced autoimmunity include molecular mimicry, alteration of lymphocyte signaling, and interference in the development of tolerance to self-antigens.
This attack on self-antigens leads to the onset of MS, which is characterized by symptoms of numbness, lack of coordination, blindness and paralysis.
More than 80 autoimmune disorders have been identified, all involving aberrant immune responses to self-antigens.
Although immune cells infiltrate tumors, they are frequently unable to mount a full-scale attack, because tolerance mechanisms prevent them from destroying cells that express self-antigens.
The ability of sCD83-treated dendritic cells to induce regulatory T cells, which are responsible for suppressing the immune system response and maintaining tolerance to self-antigens, validates Argos' program for evaluating sCD83's utility in treating transplantation rejection and a number of autoimmune disorders," commented Charles Nicolette, Ph.
When targeting activating Fc receptors, activation of TH1 and CTL leads to the breaking of tolerance to self-antigens in cancer and could also be applied presumably to chronic viral infections like hepatitis, while switching from a TH2 to TH1 type response could be developed as a novel treatment for allergy and asthma; -- When targeting to inhibitory Fc receptors, the immune response could be inactivated, extending the technology in a fundamentally different way to autoimmune diseases such as diabetes and multiple sclerosis.
The Griffiths patent relates to methods of isolating specific antibodies to human self-antigens from phage display libraries and to antibodies produced by these methods * In April 1999 MorphoSys filed a 'declaratory judgement action' in the US District Court of Washington DC, asking the Court to declare that the CAT's patent is invalid, and/or declare that it does not infringe the patent.