Dhib-Jalbut Suhayl
Department of Neurology, University of Medicine and Dentistry of New Jersey-Robert Wood Johnson Medical School, New Brunswick, NJ 08901-2160, USA.
Neurology. 2007 May 29;68(22 Suppl 3):S13-21; discussion S43-54. doi: 10.1212/01.wnl.0000275228.13012.7b.
Substantial evidence supports autoimmune activity as the etiologic mechanism underlying multiple sclerosis (MS). Both the innate and the adaptive arms of the immune system are involved in the aberrant response to several antigens associated with the myelin sheath and oligodendrocytes (OGCs) after the activation of immune cells by self- or cross-reactive microbial pathogens. The CD4(+) Th1 cell, in particular, has been implicated, but it is abetted by a variety of other cell types (CD8(+) cells, B cells, macrophages, and microglia) and soluble products (proteases, cytokines, and nitric oxide [NO]) that act both outside of and within the CNS. This review describes recent and salient findings from animal models and human clinical studies that have established our current understanding of the distinct steps in the development of immune autoreactivity that culminates in the CNS lesions associated with MS.
大量证据支持自身免疫活动是多发性硬化症（MS）的病因机制。免疫系统的固有免疫和适应性免疫分支在免疫细胞被自身或交叉反应性微生物病原体激活后，对与髓鞘和少突胶质细胞（OGC）相关的几种抗原产生异常反应中均有涉及。特别是CD4(+) Th1细胞已被牵连其中，但它还受到多种其他细胞类型（CD8(+)细胞、B细胞、巨噬细胞和小胶质细胞）以及在中枢神经系统内外起作用的可溶性产物（蛋白酶、细胞因子和一氧化氮[NO]）的协助。本综述描述了动物模型和人类临床研究的最新显著发现，这些发现确立了我们目前对免疫自身反应性发展中不同步骤的理解，这种自身反应性最终导致了与MS相关的中枢神经系统病变。
