谷氨酸受体3B亚单位抗体参与自身免疫性癫痫的研究进展  

Recent advance in glutamate receptor subunit 3 peptide B antibodies involving in antoimmune epilepsy

作　　者：张威 杨晨唯 漆星月 刘婷婷 宋晓涛 曲学彬 姚瑞芹 Zhang Wei;Yang Chenwei;Qi Xingxue;Liu Tingting;Song Xiaotao;Qu Xuebin;Yao Ruiqin(School of Life Science,Xuzhou Medical University,Xuzhou 221004,China)

机构地区：[1]徐州医科大学生命科学学院,徐州221004

出　　处：《中华神经医学杂志》2020年第4期404-407,共4页Chinese Journal of Neuromedicine

基　　金：江苏省高等学校大学生创新创业训练计划(201810313098H)。

摘　　要：自身免疫性癫痫(AE)是一类由自身抗体或免疫细胞介导的癫痫,其发病机制主要为AE相关的自身免疫性抗体作用于神经细胞膜表面或细胞内抗原,导致神经系统兴奋性和抑制性紊乱,从而引起癫痫发作。谷氨酸受体3B亚单位抗体(GluR3B Ab's)是一种与AE发作相关的抗神经元自身抗体,其与神经元或少突胶质前体细胞上的α-氨基-3-羟基-5-甲基-4-异恶唑丙酸受体(AMPAR)的GluR3B亚基结合,增加细胞内Ca2+含量导致Ca2+超载,诱发能量代谢紊乱,产生有毒代谢物质损伤神经元及少突胶质前体细胞,促使癫痫发生发展。本文主要围绕GluR3B Ab's参与AE的发生发展机制进行综述。Autoimmune epilepsy(AE)is a type of epilepsy mediated by autoantibodies and immune cells.The main pathogenesis of AE is that autoimmune antibodies related to AE interact with surface of nervous cell membrane antigens or intracellular antigens,which leads to the disorder of excitatory and inhibitory nervous system and causes epileptic seizures.Glutamate receptor subunit 3 peptide B antibodies(GluR3B Ab's)are one type of anti-neuron autoantibodies related to AE,and they can combine with GluR3B subunit ofα-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid receptor(AMPAR),which causes an increase of intracellular calcium.Intracellular calcium overload further leads to dysregulation of energy metabolism in neurons or oligodendrocyte progenitor cells(OPCs).The damage of neurons or OPCs eventually trigger seizure.Here,we mainly discuss the mechanisms of GluR3B Ab's involving in the development of autoimmune epilepsy.

关 键 词：自身免疫性癫痫 谷氨酸受体3B亚单位抗体 神经元 少突胶质前体细胞 

分 类 号：R742[医药卫生—神经病学与精神病学]