Croxford J Ludovic, Olson Julie K, Miller Stephen D
Department of Microbiology--Immunology and the Interdepartmental Immunobiology Center, Northwestern University Medical School, 303 East Chicago Avenue, 60611, Chicago, IL, USA.
Autoimmun Rev. 2002 Oct;1(5):251-60. doi: 10.1016/s1568-9972(02)00080-0.
The pathogenesis of multiple sclerosis (MS), a human demyelinating disease of the central nervous system (CNS), is currently unknown. It is widely thought that MS is an autoimmune disease which is supported by animal studies showing that myelin-specific CD4+ T cells can induce similar clinical disease in mice as observed in MS. However, the mechanism(s) of activation of these autoreactive CD4+ T cells are unknown. Although genetic susceptibility is important, other factors may be involved. Viral infections have long thought to be involved in the pathogenesis of MS although there exists little or no direct evidence implicating a role for a specific virus in MS pathogenesis. This review will discuss two models of virus-induced CNS autoimmunity, molecular mimicry and epitope spreading. These two mechanisms of activation of autoreactive T cells are presented in the context of MS.
多发性硬化症（MS）是一种中枢神经系统（CNS）的人类脱髓鞘疾病，其发病机制目前尚不清楚。人们普遍认为MS是一种自身免疫性疾病，动物研究支持这一观点，这些研究表明，髓鞘特异性CD4 + T细胞可在小鼠中诱发与MS中观察到的类似临床疾病。然而，这些自身反应性CD4 + T细胞的激活机制尚不清楚。虽然遗传易感性很重要，但可能涉及其他因素。长期以来，人们一直认为病毒感染与MS的发病机制有关，尽管几乎没有直接证据表明特定病毒在MS发病机制中起作用。本综述将讨论病毒诱导的中枢神经系统自身免疫的两种模型，即分子模拟和表位扩展。自身反应性T细胞的这两种激活机制是在MS的背景下提出的。
