Khitrov Alexander N, Shogenov Zaur S, Tretyak Eugenia B, Ischenko Anatoly I, Matsuura Eiji, Neuhaus Oliver, Paltsev Mikhail A, Suchkov Sergey V
IM Sechenov Moscow Medical Academy, Department of Pathology, Moscow, Russia.
Expert Rev Clin Immunol. 2007 May;3(3):323-31. doi: 10.1586/1744666X.3.3.323.
Autoimmunity is still a mystery of clinical immunology and medicine as a whole. The etiology and pathogenesis of autoimmune disorders remain unclear and, thus, are assessed as a balance between hereditary predisposition, triggering factors and the appearance of autoantibodies and/or self-reactive T cells. Among the immunological armamentarium, molecular mimicry, based on self-reactive T- and B-cell activation by cross-reactive epitopes of infectious agents, is of special value. Hypotheses regarding the possible involvement of molecular mimicry in the development of postinfectious autoimmunity are currently very intriguing. They provide new approaches for identifying etiological agents that are associated with postinfectious autoimmunity, paired microbial- and tissue-linked epitopes targeted for autoimmune reaction determination, postinfectious autoimmunity pathogenesis recognition and specific prevention, and therapy for autoimmune disorder development.
自身免疫仍然是临床免疫学乃至整个医学领域的一个谜。自身免疫性疾病的病因和发病机制仍不明确,因此,被认为是遗传易感性、触发因素以及自身抗体和/或自身反应性T细胞出现之间的一种平衡。在免疫武器库中,基于感染因子的交叉反应表位激活自身反应性T细胞和B细胞的分子模拟具有特殊价值。目前,关于分子模拟可能参与感染后自身免疫发展的假说非常引人入胜。它们为识别与感染后自身免疫相关的病原体、确定针对自身免疫反应的成对微生物和组织相关表位、认识感染后自身免疫发病机制以及特异性预防和治疗自身免疫性疾病的发展提供了新方法。