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Toll样受体在格林-巴利综合征发病机制中的作用

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摘要 格林-巴利综合征(Guillain-Barre syndrome,GBS)又称急性炎症性脱髓鞘性多发性神经根炎,是累及周围神经的自身免疫性脱髓鞘疾病,主要病理改变是脱髓鞘和炎性浸润。临床上呈急性或亚急性发病,以迅速进展的肢体无力、腱反射减弱、肌张力降低为特征,是世界范围内引起急性弛缓性瘫痪的常见病因。目前多认为是由感染等因素诱导、细胞及体液免疫共同介导的自身免疫性疾病,其确切发病机制尚未完全阐明。Toll 样受体(Toll like receptor,TLR)是一种模式识别受体,可以识别病原微生物的保守抗原分子,如脂多糖、肽聚糖等。Toll 样受体信号的过度活化可打破机体对自身抗原的免疫耐受,参与自身免疫性疾病的发生。近年来研究发现 Toll 样受体家族(TLRs )在 GBS 发病及发展过程中具有重要作用。本文综述了 TLRs 及其信号通路在 GBS 发病机制中的作用,重点介绍 TLR2,4,9在GBS 发病机制中的作用。
出处 《中国医药生物技术》 2013年第6期456-459,共4页 Chinese Medicinal Biotechnology
基金 首都医科大学基础临床合作课题 北京市卫生系统高层次卫生技术人才培养项目
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