Multiple sclerosis immunology The healthy immune system vs the MS immune system
Multiple sclerosis immunology The healthy immune system vs the MS immune system
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DOI：
10.1212/wnl.0b013e3181c97c8f
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发表时间：
2010-01-05
期刊：
影响因子：
9.9
通讯作者：
Shoemaker, Jennifer
中科院分区：
文献类型：
--
作者：
Kasper, Lloyd H.;Shoemaker, Jennifer
多发性硬化症（MS）是一种使人衰弱的自身免疫性疾病，其特征是炎症和轴突变性。由此产生的脱髓鞘和随后的轴突变性导致了多发性硬化症患者的残疾。早期研究表明疾病进展是由CD4(+)效应T细胞驱动的。然而，专门针对这些细胞的临床疗法在很大程度上并不有效。因此，实验性自身免疫性脑脊髓炎（多发性硬化症的实验模型）和人类多发性硬化症的新研究领域已经确定了以前未知的对疾病发病机制的贡献，包括产生白细胞介素17的辅助性T细胞17、B细胞、CD8+T细胞以及CD4+和CD8+T调节细胞。对这些细胞各自作用机制的研究已经确定了对抗这种毁灭性疾病的新治疗靶点。本文回顾了多发性硬化症患者与非多发性硬化症患者的自身免疫反应，并总结了多发性硬化症患者和非多发性硬化症患者之间免疫反应的根本差异。对这些自身免疫差异和免疫系统稳态平衡破坏的研究将有助于指导未来对多发性硬化症治疗的研究，特别是关注这种疾病的长期管理。神经病学2010;74（增刊1）：S2-S8
Multiple sclerosis (MS) is a debilitating autoimmune disease characterized by both inflammation and axonal degeneration. The resulting demyelination and subsequent degeneration of axons account for the disability of patients with MS. Early investigations indicated that disease progression was driven by CD4(+) effector T cells. However, clinical therapies specifically targeting these cells have, for the most part, not been effective. Therefore, new areas of research in experimental autoimmune encephalomyelitis (the experimental model of MS) and human MS have identified previously unknown contributions to disease pathogenesis, including interleukin-17-producing T helper 17 cells, B cells, CD8(+) T cells, and both CD4(+) and CD8(+) T-regulatory cells. Research into the respective mechanisms of action of these cells has identified novel therapeutic targets to combat this devastating disease. This article reviews the autoimmune response in patients with MS compared with individuals without MS and summarizes the fundamental differences in the immunologic response between people with and without MS. Investigations into these autoimmune differences and the disruption of the homeostatic balance of the immune system will help guide future research into MS therapeutics, with particular attention to the long-term management of this disease. NEUROLOGY 2010;74(Suppl1):S2-S8