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Multiple sclerosis pathogenesis: missing pieces of an old puzzle

机译:多发性硬化症发病机制:缺少旧拼图的碎片

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Traditionally, multiple sclerosis (MS) was considered to be a CD4 T cell-mediated CNS autoimmunity, compatible with experimental autoimmune encephalitis model, which can be characterized by focal lesions in the white matter. However, studies of recent decades revealed several missing pieces of MS puzzle and showed that MS pathogenesis is more complex than the traditional view and may include the following: a primary degenerative process (e.g. oligodendroglial pathology), generalized abnormality of normal-appearing brain tissue, pronounced gray matter pathology, involvement of innate immunity, and CD8 T cells and B cells. Here, we review these findings and discuss their implications in MS pathogenesis.
机译:传统上,多发性硬化症(MS)被认为是CD4 T细胞介导的CNS自身免疫,与实验性自身免疫性脑炎模型相容,可以通过白质的焦点表征。 然而,近几十年的研究揭示了几个缺失的MS谜题,并且表明MS发病机制比传统观点更复杂,并且可以包括以下内容:初级退行性过程(例如少突畸形病理学),正常出现的脑组织的广义异常, 发音灰质病理学,先天免疫和CD8 T细胞和B细胞的累积。 在这里,我们审查了这些调查结果并讨论了他们对MS发病机制的影响。

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