autoimmunity

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autoimmunity

 [aw″to-ĭ-mu´nĭ-te]
a condition characterized by a specific humoral or cell-mediated immune response against the constituents of the body's own tissues (autoantigens); it may result in hypersensitivity reactions or, if severe, in autoimmune disease.

au·to·im·mu·ni·ty

(aw'tō-i-myū'ni-tē),
In immunology, the condition in which one's own tissues are subject to deleterious effects of actions of the immune system, as in autoallergy and in autoimmune disease; specific humoral or cell-mediated immune response against the body's own tissues. Synonym(s): autoallergy

autoimmunity

The reaction of a host organism’s immune system to self-antigens as if they were foreign. It is characterised by T-cell activation, clonal expansion and antibody production against tissues, cells and antigens, which results in autoimmune disease.

autoimmunity

Self immunity Immunology The reaction of an organism's immune system to self antigens as if they were non-self or foreign; like alloimmunity, autoimmunity is characterized by the activation of T cells, clonal expansion, and antibody production. See Anti-nuclear antibodies, Anti-receptor antibodies, Clonal anergy, Superantigen.

au·to·im·mu·ni·ty

(aw'tō-i-myū'ni-tē)
immunology The condition in which one's own tissues are subject to deleterious effects of the immune system, as in autoallergy and in autoimmune disease; immune response against the body's own tissues.
See: autoallergy

autoimmunity

a situation where the immunological defences of the body become sensitized to parts of the same body resulting in self-destruction in that area. In other words, ‘self ANTIGENS become mistaken for ‘foreign’ antigens, so setting up an IMMUNE RESPONSE. Such an occurrence is clearly dangerous and may be associated with ageing. An example is rheumatoid arthritis in humans.

Autoimmunity

A condition in which the body's immune system produces antibodies in response to its own tissues or blood components instead of foreign particles or microorganisms.
Mentioned in: AIDS, Hypoparathyroidism

au·to·im·mu·ni·ty

(aw'tō-i-myū'ni-tē)
In immunology, the condition in which one's own tissues are subject to deleterious effects of actions of the immune system.
References in periodicals archive ?
A putative homologue of the human autoantigen Ku from Saccharomyces serevisiae.
CII is a strong candidate autoantigen relevant to RA, because of its abundance in cartilage and because of its ability to trigger immune mediated destructive polyarthritis in rodents and primates.11 There have been few studies on T cell immunity to CII in RA12,13 but the findings are variable.
The fact that Ts cells can be produced by dermatological immunization may have important implications for the design of therapeutic protocols that aimed at regulating the immune response to autoantigens in autoimmune diseases.
Initial infiltration of the islets requires autoantigen recognition by the dendritic cells (DCs) and macrophages, which are professional APC.
Vivekanandan-Giri et al., "NETs are a source of citrullinated autoantigens and stimulate inflammatory responses in rheumatoid arthritis," Science Translational Medicine, vol.
The approach we present here is based on inducing peripheral tolerance using a synthetic peptide derived from sequences of multiple prevalent citrullinated autoantigens. Indeed, the citrullinated [beta]-fibrinogen peptide was also able to immunomodulate immune cells of RA patients even if to a limited extent compared to the Cit-ME peptide.
In contrast, because many of these proteins are sequestered intracellular proteins, the presence of immune effectors in situ or following translocation to peripheral lymphoid tissue (i.e., cervical lymph nodes and spleen) results in a humoral immune response directed against these autoantigens. With the development of immunological memory (IgG) or chronic degeneration (IgM), these immunoglobulins are likely to persist.
"Islet autoantibody" is a generic term for any one of a group of autoantibodies that are directed against the islets of Langerhans or, in some circumstances, are directed specifically against autoantigens of the insulin-secreting [beta] cells.
Among several approaches to prevention of T1D, "vaccination" using islet autoantigens (intact or altered peptides derived from insulin, GAD65 or other proteins) stands out as potentially inducing long-term tolerance by induction of regulatory T cells that down-regulate immunity to autoantigens.
Among several approaches to prevention of Type 1 diabetes (T1D), "vaccination" using islet autoantigens (intact or altered peptides derived from insulin, [GAD.sub.65] or other proteins) stands out as potentially inducing long-term tolerance by induction of regulatory T cells that downregulate immunity to autoantigens.
B cells may theoretically participate in the immune dysregulation of SLE at multiple levels by: (1) serving as the precursors of antibody-secreting cells, (2) taking up and presenting autoantigens to T cells, (3) helping to regulate and organize inflammatory responses through cytokine and chemokine secretion (such as interleukin-10, interleukin-6, interferon-[gamma], and lymphotoxin-[alpha]), and (4) regulating other immune cells.