多发性硬化症的发病机制:自身免疫有多大作用?

Walter Fierz
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引用次数: 0

摘要

多发性硬化症(MS)通常被认为是一种自身免疫性疾病,主要是因为该疾病的首选和研究充分的动物模型是自身免疫性模型。然而,在人类疾病中,长期以来一直在寻找MS自身免疫的证据,结果甚微。另一方面,EBV和HHV-6A两种病毒发挥了etio-致病性作用,正如最近讨论的那样,它们之间的相互作用可能是MS发病机制的关键因素。这篇简短的综述总结了支持这一观点的证据,该观点将MS的etio-发病机制从自身免疫转变为病毒。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Pathogenesis of Multiple Sclerosis: How Much Space is Left for Autoimmunity?
Multiple Sclerosis (MS) is generally considered an autoimmune disease, mainly because the preferred and wellstudied animal models for the disease are autoimmune models. In human disease, however, evidence for autoimmunity in MS has been sought for a long time with marginal results. On the other hand, two viruses, EBV and HHV-6A, play an etio-pathogenic role and, as recently discussed, their mutual interaction might be a key element in the pathogenesis of MS. This short review summarizes evidence that supports this view of changing the paradigm about the etio-pathogenesis of MS from autoimmunity to viral.
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