神经小胶质细胞在EAE脱髓鞘和髓鞘再生中的作用机制进展  

Advances in mechanisms of microglial function on demyelination and remyelination in EAE model

作　　者：叶妮 李国陵[2] 程晓东 YE Ni;LI Guo-Ling;CHENG Xiao-Dong(Institute of Clinical Immunology,Yueyang Hospital of Integrated Traditional Chinese and Western Medicine,Shanghai University of Traditional Chinese Medicine,Shanghai 200437,China)

机构地区：[1]上海中医药大学附属岳阳中西医结合医院临床免疫研究所,上海200437 [2]上海中医药大学附属岳阳中西医结合医院风湿免疫科, 上海200437

出　　处：《中国免疫学杂志》2018年第4期602-608,共7页Chinese Journal of Immunology

基　　金：本文为国家自然科学基金面上项目(81173630、81673669、81703782)和上海中医药大学高峰学科建设项目(30304114323)。

摘　　要：炎性细胞浸润和脱髓鞘是中枢神经系统(CNS)的自身免疫性疾病——多发性硬化(MS)的主要病理特征,相关的病理研究多在其动物模型实验性自身免疫性脑脊髓膜炎(EAE)中开展。神经小胶质细胞(MG)是CNS的主要免疫效应细胞,EAE时它的激活在脱髓鞘和髓鞘再生中表现出复杂的作用。M1型MG是导致脱髓鞘的重要原因,抑制髓鞘再生;而M2型MG可以促进髓鞘再生,抵抗脱髓鞘。本文综述MG在EAE脱髓鞘和髓鞘再生中的直接作用机制,及其通过星形胶质细胞产生的间接作用机制及进展。Inflammatory cells infiltration and demyelination in the central nervous system(CNS)are the main pathological characteristics of multiple sclerosis(MS),an autoimmune disease in the CNS.Most of the related pathological studies are carried out in the animal model experimental autoimmune encephalomyelitis(EAE).Microglia(MG)are the primary immune effector cells of the CNS and their activation can play complex roles in demyelination and remyelination during EAE.In detail,M1 phenotype is an important cause of demyelination and detrimental to remyelination while M2 phenotype can promote remyelination and inhibit demyelination.In this review,we not only focus on advances in the direct mechanisms of microglial function on demyelination and remyelination in EAE model,also the indirect mechanisms by astrocytes.

关 键 词：神经小胶质细胞 实验性自身免疫性脑脊髓膜炎 多发性硬化 脱髓鞘 髓鞘再生 

分 类 号：R363.21[医药卫生—病理学]