Self-Recognition (Tolerance)
المؤلف:
Mary Louise Turgeon
المصدر:
Immunology & Serology in Laboratory Medicine
الجزء والصفحة:
5th E, P385-386
2025-09-17
347
In the initial stage of some diseases, infiltration by T lymphocytes may induce inflammation and tissue damage, leading to alterations in self antigens and production of autoantibodies. In other diseases, only the production of autoantibodies is noted with tissue damage. These autoantibodies attack cell sur face antigens or membrane receptors or combine with antigen to form immune complexes that are deposited in tissue, subsequently causing complement activation and inflammation.
An immune response requires presentation of a foreign anti gen by an antigen-presenting cell (APC) and another signal from the appropriate major histocompatibility complex (MHC) molecule on the host’s cells. Both are needed for an immune response. Tolerance is the lack of immune response to self anti gens and is initiated during fetal development (central tolerance) by the elimination of cells with the potential to react strongly with self antigens. Peripheral tolerance is a process involving mature lymphocytes and occurs in the circulation. Central tolerance develops in the thymus during fetal life. Self antigens are presented by dendritic cells to self-reactive T cells that are responsible for positive and negative selection of specific lymphocytes. The ultimate goal is to remove T lymphocytes that respond strongly to self antigens. As genes rearrange and code for antigen receptors, the T cell receptors (TCRs) produced may or may not be specific for the MHC expressed on that individual’s cells. Positive selection cells that have TCRs capable of responding with self antigens (low-level MHC affinity) are selected for continued growth.
Self-recognition (tolerance) is induced by at least two mechanisms involving contact between antigen and immunocompetent cells:
• Elimination of the small clone of immunocompetent cells programmed to react with the antigen (Burnet’s clonal selection theory)
• Induction of unresponsiveness in the immunocompetent cells through excessive antigen binding to them and triggering of a suppressor mechanism
The normal immune response is modulated by antigen specific and antigen-nonspecific suppressor cell activity.
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