Immunopathogenesis and treatment of myasthenia gravis.
Immunopathogenesis and treatment of myasthenia gravis.
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重症肌无力的免疫发病机制和治疗。
DOI：
10.1007/bf00915723
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发表时间：
1987
影响因子：
9.1
通讯作者：
Lisak,RP
中科院分区：
文献类型：
--
作者：
Levinson,AI;Zweiman,B;Lisak,RP
重症肌无力（MG）4是一种以横纹肌无力为特征的神经肌肉传递疾病。神经肌肉传递的缺陷是由自身抗体介导的，其与突触后肌神经接头处的烟碱乙酰胆碱（AChR）受体反应。在这篇综述中，我们研究了MG的免疫发病机制，并考虑在这一领域的工作以及我们对免疫调节和自身免疫的理解的进展所建议的各种治疗策略。
Myasthenia gravis (MG) 4 is a disease of neuromuscular transmission characterized by weakness of striated muscles. The defect in neuromuscular transmission is mediated by autoantibodies which react with nicotinic acetycholine (AChR) receptors at postsynaptic myoneural junctions. In this review, we examine the immunopathogenesis of MG and consider various therapeutic strategies suggested by work in this area as well as by advances in our understanding of immunoregulation and autoimmunity.