Pathogenesis of multiple sclerosis: an update on immunology
Pathogenesis of multiple sclerosis: an update on immunology
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DOI：
10.1097/00019052-200206000-00001
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发表时间：
2002-06-01
影响因子：
4.8
通讯作者：
Sommer, N
中科院分区：
文献类型：
--
作者：
Hemmer, B;Cepok, S;Sommer, N
多发性硬化症的特征是中枢神经系统的脱髓鞘和慢性炎症。在实验性自身免疫性脑脊髓炎动物模型中的广泛研究表明，多发性硬化症是一种由髓鞘特异性CD4 T细胞介导的自身免疫性疾病，其分泌T辅助细胞1型细胞因子和特纳坏死因子α。这一概念已被广泛用于开发新的实验疗法。然而，最近的研究结果在实验性自身免疫性脑脊髓炎和多发性硬化症的问题，一个简单的CD4辅助性T细胞1型T细胞的范例，并提供证据的作用，各种免疫细胞在实验性自身免疫性脑脊髓炎和多发性硬化症的发病机制。在本文中，我们回顾了最近的进展，并讨论了新的治疗策略的影响。
Multiple sclerosis is characterized by demyelination and chronic inflammation of the central nervous system. Extensive studies in the animal model experimental autoimmune encephalomyelitis have suggested that multiple sclerosis is an autoimmune disorder mediated by myelin-specific CD4 T cells secreting T helper type 1 cytokines and turner necrosis factor alpha. This concept has been widely used to develop new experimental therapies. However, recent findings in both experimental autoimmune encephalomyelitis and multiple sclerosis question a simple CD4 T helper type 1 T cell paradigm and provide evidence for the role of various immune cells in the pathogenesis of experimental autoimmune encephalomyelitis and multiple sclerosis. In this paper we review recent progress and discuss the implications for new therapeutic strategies.