Molecular Mimicry: Its Evolution from Concept to Mechanism as a Cause of Autoimmune Diseases
Molecular Mimicry: Its Evolution from Concept to Mechanism as a Cause of Autoimmune Diseases
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DOI：
10.1089/mab.2013.0090
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发表时间：
2014-06-01
影响因子：
--
通讯作者：
Oldstone, Michael B. A.
中科院分区：
文献类型：
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作者：
Oldstone, Michael B. A.
在克隆水平上，某些抗体和T细胞可以与微生物和宿主细胞中发现的不同抗原相互作用。来自多种RNA和DNA病毒以及大量T细胞克隆的800多种单克隆抗体中，超过5%参与这种相互作用。我们称之为分子模拟的几种交叉反应是针对参与自身免疫反应和疾病的独特宿主蛋白。因此，作为宿主对病毒或微生物感染的应答而启动的分子模拟，但可替代地与适当的宿主抗原交叉反应，可以是引发自身免疫性疾病的机制。分子模拟提供了一个解释的遗传观察，同卵双胞胎很少表现出相同的自身免疫性疾病和记录的流行病学证据，微生物和/或病毒感染往往先于自身免疫性疾病。
On a clonal level, certain antibodies and T cells can interact with dissimilar antigens found in microbes and in host cells. More than 5% of over 800 monoclonal antibodies derived from multiple RNA and DNA viruses, as well as from a large number of T cell clones, engage in such interactions. Several of these cross-reactions, which we termed molecular mimicry, are against unique host proteins involved in autoimmune responses and diseases. Thus, molecular mimicry initiated as a host response to a virus or a microbial infection, but alternatively cross-reacting with an appropriate host-antigen, can be a mechanism for instigating an autoimmune disease. Molecular mimicry provides an explanation for the genetic observation that identical twins rarely manifest the same autoimmune disease and the documented epidemiologic evidence that microbial and/or viral infections often precede autoimmune disorders.