Molecular mimicry, microbial infection, and autoimmune disease: evolution of the concept.
Molecular mimicry, microbial infection, and autoimmune disease: evolution of the concept.
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DOI：
10.1007/3-540-30791-5_1
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发表时间：
2005
影响因子：
--
通讯作者：
Oldstone MB
中科院分区：
文献类型：
--
作者：
Oldstone MB
分子模拟是指来自不同基因的分子或其蛋白质产物所具有的相似结构。几个线性氨基酸或它们的构象拟合可能是共享的，即使它们的起源是分开的。因此，在病毒或微生物感染期间，如果该生物体与宿主共享B或T细胞的交叉反应性表位，则对感染因子的反应也将攻击宿主，引起自身免疫性疾病。这一主题的一种变化是当第二次、第三次或重复感染与第一次（起始）病毒但不一定是宿主共享交叉反应性B或T细胞表位时。在这种情况下，继发感染因子增加了增强或促进自身免疫攻击的抗病毒/抗宿主效应抗体或T细胞的数量。这一概念的形成，最初通过研究单克隆抗体或克隆T细胞的体外交叉识别，通过其在体内的动物模型和选定的人类疾病的演变进行了探讨，在这个小型审查。
Molecular mimicry is defined as similar structures shared by molecules from dissimilar genes or by their protein products. Either several linear amino acids or their conformational fit may be shared, even though their origins are separate. Hence, during a viral or microbe infection, if that organism shares cross-reactive epitopes for B or T cells with the host, then the response to the infecting agent will also attack the host, causing autoimmune disease. A variation on this theme is when a second, third, or repeated infection(s) shares cross-reactive B or T cell epitopes with the first (initiating) virus but not necessarily the host. In this instance, the secondary infectious agents increase the number of antiviral/antihost effector antibodies or T cells that potentiate or precipitate the autoimmune assault. The formation of this concept initially via study of monoclonal antibody or clone T cell cross-recognition in vitro through its evolution to in vivo animal models and to selected human diseases is explored in this mini-review.