α-微管蛋白乙酰化调控NLRP3炎症小体活化的研究进展  

Research progress of regulation of NLRP3 inflammasome activation byα-tubulin acetylation

作　　者：李陈广 吴晓君 肖礼祖(指导) LI Chenguang;WU Xiaojun;XIAO Lizu(Huazhong University of Science and Technology Union Shenzhen Hospital,Shenzhen 518052,China)

机构地区：[1]华中科技大学协和深圳医院,深圳518052

出　　处：《中国免疫学杂志》2023年第2期427-433,共7页Chinese Journal of Immunology

基　　金：中国博士后基金面上项目(2021M702276)。

摘　　要：NLRP3炎症小体在固有免疫系统中发挥重要作用,介导caspase-1激活并促进炎症因子IL-1β分泌应答机体的病原微生物感染和细胞损伤,但异常活化的NLRP3炎症小体也会导致多种炎症性疾病的发生。NLRP3炎症小体的激活涉及多种细胞内分子和信号通路,导致细胞内离子流动变化、线粒体功能紊乱和溶酶体损伤等一系列事件发生,然而NLRP3炎症小体组装的详细调控机制尚不清楚。本综述着重介绍α-微管蛋白的乙酰化介导线粒体通过动力蛋白转运到内质网附近,从而促进线粒体上的ASC与内质网上的NLRP3接触,诱导NLRP3炎症小体组装。NLRP3 inflammasome is a critical component of innate immune system that mediates caspase-1 activation and secretion of proinflammatory cytokines IL-1βin response to microbial and cellular damage.However,aberrant activation of NLRP3 inflammasome has been involved in several inflammatory diseases.NLRP3 inflammasome is activated by diverse stimuli,and multiple molecular and cellular events,including ionic flux,mitochondrial dysfunction,and lysosomal damage have been shown to trigger its activation.However,NLRP3 responds to those signaling events and initiates the assembly of NLRP3 inflammasome is not fully understood.In this review,we focus on research progress of acetylatedα-tubulin mediates dynein-dependent transportation of mitochondria to an area near the endoplasmic reticulum,which in turn enhances the contact of ASC on mitochondria with NLRP3 on endoplasmic reticulum,resulting in the assembly of NLRP3 inflammasome.

关 键 词：Α-微管蛋白 乙酰化 NLRP3炎症小体 固有免疫 

分 类 号：R392.1[医药卫生—免疫学]