摘要
固有免疫是宿主细胞防御病毒感染的第一道防线,Toll样受体(TLR)、维甲酸诱导基因Ⅰ样受体(RLRs)等模式识别受体(PRRs)在其中发挥重要作用。病毒感染机体后,PRRs介导的信号通路中的线粒体抗病毒信号蛋白(MAVS)作为下游信号传递的共同接头分子可接收上游TLR、RIG-Ⅰ传递的信号,活化下游NF-κB和IRF3/7信号通路,进而激活干扰素(IFN)的表达,在固有免疫信号通路中起“桥梁”作用。越来越多的研究表明,病毒在长期进化过程中已进化出一系列逃逸固有免疫应答的机制,可通过干扰MAVS介导的信号通路中的多个位点来逃避宿主的抗病毒免疫应答,从而完成病毒自身的复制增殖。本文综述了MAVS在Ⅰ型IFN通路中作用及其在抗DNA病毒和RNA病毒反应机制中的最新研究进展,为研究MAVS抗病毒的分子机制提供理论参考。
Innate immunity is the first line of the host cell defensing against viral infection,in which the pattern recognition re-ceptors(PRRs)such as Toll-like receptors(TLRs)and retinoic acid induces geneⅠ-like receptors(RLRs)play an important role.After virus infection,mitochondrial antiviral signaling protein(MAVS)in PRRs-mediated signaling pathway,which are of the com-mon linker molecule for downstream signal transmission,can receive signals transmitted by upstream TLR and RIG-Ⅰ,activate down-stream NF-κB and IRF3/7 signaling pathways leading to the activation of interferon(IFN)expression.Therefore MAVS acts as a bridge in the innate immune signaling pathway.More and more studies have shown that viruses have evolved a series of mechanism to escape the innate immune response over the long course of their evolution,and evaded the host's antiviral immune response by interfer-ing with multiple sites in the MAVS-mediated signaling pathway so as to complete its own replication and proliferation.In this paper,the role of MAVS in IFN-Ⅰpathway and its latest research progress in the mechanism of anti-DNA viruses and anti-RNA viruses reac-tion are reviewed,providing theoretical basis for further studying the detailed mechanism of anti-virus of MAVS.
作者
毕冬琳
杨晓莉
杨东亮
刘方程
张潇文
李琼毅
柏家林
BI Donglin;YANG Xiaoli;YANG Dongliang;LIU Fangcheng;ZHANG Xiaowen;LI Qiongyi;BAI Jialin(Key Laboratory of Bioengineering and Technology of National Ethnic Affairs Commission,Biomedical Research Center,Northwest Minzu University,Lanzhou 730030,China)
出处
《中国免疫学杂志》
CAS
CSCD
北大核心
2024年第11期2452-2457,2464,共7页
Chinese Journal of Immunology
基金
国家自然科学基金(31860696,31702234)。
关键词
线粒体抗病毒信号蛋白
固有免疫
病毒感染
免疫逃逸
Mitochondrial antiviral signaling proteins
Innate immunity
Viral infections
Immune escape