Abstract
Acquisition of a complex immune system during evolution provided organisms with the most effective defense mechanism against “foreign” or “non-self” invaders. This efficient protection against pathogens, however, has been achieved at the expense of a higher risk for “self reaction or autoimmunity. Establishment of self-tolerance and homeostasis in the immune system is regulated at different physiological stages of immune cells development. The breakdown in discrimination between “self” and “non-self”causes an aberrant immune response against autoantigens that promote damage to the “self” cells and tissue(s), resulting in various autoimmune phenotypes. Whereas activation and clonal proliferation of autoreactive T- and B- lymphocytes underlies the pathogenesis of autoimmune diseases, the mechanism by which self-tolerance is lost and autoimmune responses are induced is not clear yet. Autoimmunity is a multi-step process that occurs as a consequence of complex interaction between genetic susceptibility and non-genetic factors. Programmed cell death, as a key mechanism to regulate immune system function, has a crucial influence on both the selection process of immune cells and the maintenance of this immune tolerance in peripheral repertoire. Thus, defects in apoptotic death pathways may contribute to the development of autoimmune response in susceptible individuals in certain conditions.
Keywords: Autoimmunity, apoptosis, autoantigen, autoantibody, adaptive immune response, innate immune system, tolerance
Current Medicinal Chemistry
Title: Autoimmunity and Apoptosis - Therapeutic Implications
Volume: 14 Issue: 29
Author(s): Iran Rashedi, Soumya Panigrahi, Peyman Ezzati, Saeid Ghavami and Marek Los
Affiliation:
Keywords: Autoimmunity, apoptosis, autoantigen, autoantibody, adaptive immune response, innate immune system, tolerance
Abstract: Acquisition of a complex immune system during evolution provided organisms with the most effective defense mechanism against “foreign” or “non-self” invaders. This efficient protection against pathogens, however, has been achieved at the expense of a higher risk for “self reaction or autoimmunity. Establishment of self-tolerance and homeostasis in the immune system is regulated at different physiological stages of immune cells development. The breakdown in discrimination between “self” and “non-self”causes an aberrant immune response against autoantigens that promote damage to the “self” cells and tissue(s), resulting in various autoimmune phenotypes. Whereas activation and clonal proliferation of autoreactive T- and B- lymphocytes underlies the pathogenesis of autoimmune diseases, the mechanism by which self-tolerance is lost and autoimmune responses are induced is not clear yet. Autoimmunity is a multi-step process that occurs as a consequence of complex interaction between genetic susceptibility and non-genetic factors. Programmed cell death, as a key mechanism to regulate immune system function, has a crucial influence on both the selection process of immune cells and the maintenance of this immune tolerance in peripheral repertoire. Thus, defects in apoptotic death pathways may contribute to the development of autoimmune response in susceptible individuals in certain conditions.
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Cite this article as:
Rashedi Iran, Panigrahi Soumya, Ezzati Peyman, Ghavami Saeid and Los Marek, Autoimmunity and Apoptosis - Therapeutic Implications, Current Medicinal Chemistry 2007; 14 (29) . https://dx.doi.org/10.2174/092986707782793952
DOI https://dx.doi.org/10.2174/092986707782793952 |
Print ISSN 0929-8673 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-533X |
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