Research advancement in immunopathogenesis of myasthenia gravis  

重症肌无力的免疫发病机制研究进展(英文)

作　　者：黄莎[1] 谭利明[1] 

机构地区：[1]中南大学湘雅附二医院神经内科,长沙410011

出　　处：《Neuroscience Bulletin》2010年第1期85-89,共5页神经科学通报（英文版）

摘　　要：Myasthenia gravis （MG） is an autoimmune neuromuscular junction disease mediated by antibodies against the acetylcholine receptor （AChR）. The etiology and immunopathogenesis of MG remain unclear. Recent research has shown the involvement of autoantibodies, lymphocytes, cytokines and chemokines, in the pathogenesis of MG. Systematic factors are also demonstrated, such as inheritance and endocrine. This review indicates the research development in immunopathogenesis of MG.重症肌无力是一种由抗乙酰胆碱受体的抗体介导的神经肌肉接头处的自身免疫病。其发病机制尚未阐明。自身抗体、淋巴细胞免疫调节紊乱、细胞因子表达失衡及系统因素在重症肌无力的发病机制中均起重要作用。本综述旨在探讨重症肌无力的免疫学发病机制。

关 键 词：myasthenia gravis immunological pathogenesis 

分 类 号：R746.1[医药卫生—神经病学与精神病学]