Induction, acceleration or prevention of autoimmunity by molecular mimicry
Induction, acceleration or prevention of autoimmunity by molecular mimicry
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DOI：
10.1016/j.molimm.2003.11.014
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发表时间：
2004-02-01
影响因子：
3.6
通讯作者：
von Herrath, MG
中科院分区：
文献类型：
--
作者：
Christen, U;von Herrath, MG
获得性免疫系统识别的自身决定因素与微生物之间的交叉反应可能导致自身免疫性疾病的假说是非常有趣的。然而，在人类中很难获得确切的证据，而且证据往往是间接的。因此，动物模型有助于理解，如何以及何时模仿可能参与自身免疫的发病机制。在这篇文章中，我们将讨论实验场景，其中外来和自我决定因素之间的模仿本身不会引起疾病，而是使预先存在的亚临床自身免疫性疾病恶化。我们想提出，分子模拟更有可能影响已经存在的自身免疫过程，而不是从一开始就破坏耐受性而引发新的疾病。已经激活的自身反应性细胞可能比幼稚淋巴细胞更容易被交叉反应性配体重新激活并启动效应子功能。(C)2003 Elsevier Ltd.保留所有权利。
The hypothesis that cross-reactivity between microbial and self determinants recognized by the adaptive immune system could induce autoimmune diseases is very intriguing. However, definite proof in humans is very difficult to achieve and evidence is frequently circumstantial. Therefore, animal models are instrumental for understanding, how and when mimicry could be involved in the pathogenesis of autoimmunity. In this article, we will discuss experimental scenarios, where mimicry between foreign and self determinants does not cause disease per se, but rather aggravates a pre-existing yet sub-clinical autoimmune condition. We would like to propose that molecular mimicry is more likely to impact on an already existing autoimmune process rather than precipitate novel disease by breaking of tolerance from the beginning. Already activated autoreactive cells might be easier re-activated and primed for effector functions by cross-reactive ligands than naive lymphocytes. (C) 2003 Elsevier Ltd. All rights reserved.