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作 者:杜姝姝 刘文慧[1] 赵黎丽 刘熔增 DU Shushu;LIU Wenhui;ZHAO Lili;LIU Rongzeng(School of Basic Medical Science,Henan University of Science and Technology,Luoyang 471023,China)
机构地区:[1]河南科技大学基础医学院,河南洛阳471023
出 处:《中国比较医学杂志》2023年第2期119-125,共7页Chinese Journal of Comparative Medicine
基 金:国家自然科学基金(81901663);河南科技大学大学生研究训练计划项目(2021308)。
摘 要:1型发作性睡病(narcolepsy type 1,NT1)是由下丘脑食欲素(hypocretin,HCRT)神经元缺失引起的一种罕见的睡眠障碍,其主要症状是白天极度嗜睡、猝倒和睡眠紊乱。遗传和环境因素在发作性睡病的发病机制中起着至关重要的作用,特别是携带HLA-DQB1*06:02等位基因的个体。大量的遗传学和流行病学证据指向免疫系统,甲型H1N1感染或接种疫苗后,发作性睡病的发病率显著增加,提示H1N1可能是NT1的环境触发因素,但免疫系统引起HCRT神经元破坏的机制尚不清楚。NT1患者中已经检测到靶向HCRT神经元的自身反应性T细胞,其中辅助性CD4^(+)T细胞和细胞毒性CD8^(+)T细胞可能具有致病性,表明NT1的发病机制与T细胞介导的自身免疫有关。本文对T细胞介导NT1发病机制的最新研究进展作一综述。Narcolepsy type 1,which is caused by loss of hypothalamic orexin-producing neurons,is a rare sleep disorder characterized by excessive daytime sleepiness,cataplexy,and sleep disorders.Genetic and environmental factors play a major role in the pathogenesis of narcolepsy,especially in people with HLA-DQB1∗06:02 alleles.Substantial genetic and epidemiological evidence points to the immune system,for instance,a significantly increased incidence of narcolepsy was seen after the pandemic H1N1 influenza and vaccination,suggests that H1N1 may contribute to the development of NT1,but the exact mechanism of hypothalamic neuron injury by the immune system is not well understood.Autoreactive T cells against orexin neurons have been detected in samples of patients with NT1,in which helper CD4^(+)T cells and cytotoxic CD8^(+)T cells may be pathological,indicating that NT1 pathogenesis is related to T cell-mediated autoimmunity.This article reviews the recent research progress in the pathogenesis of narcolepsy type 1 induced by T cells.
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