内质网应激和未折叠蛋白反应在病毒感染及相关免疫反应中的作用  

Effects of endoplasmic reticulum stress and unfolded protein response on viral infections and related immune responses

作　　者：吴婧琦 王燕[1] 钟照华[1] Wu Jingqi;Wang Yan;Zhong Zhaohua(Department of Microbiology,Harbin Medical University,Harbin 150081,China)

机构地区：[1]哈尔滨医科大学微生物学教研室,哈尔滨150081

出　　处：《国际免疫学杂志》2022年第3期286-293,共8页International Journal of Immunology

基　　金：国家自然科学基金(81871652,82072278,81772188)。

摘　　要：内质网是真核细胞中蛋白质合成、折叠、修饰和分类的主要细胞器。病毒感染通常会干扰内质网的稳态,并导致内质网应激(endoplasmic reticulum stress,ERS)。作为一种细胞的自我保护机制,内质网会激活未折叠蛋白反应(unfolded protein response,UPR),通过减少内质网蛋白产生、增强蛋白折叠能力、促进内质网相关蛋白降解(endoplasmic reticulum-related protein degradation,ERAD)等途径减轻细胞应激压力。病毒感染诱导的ERS可以通过UPR激活宿主的免疫应答和炎症反应,影响病毒感染进程。文章概述了UPR与宿主免疫反应在病毒感染中的作用,重点描述了病毒感染相关ERS及相关炎症反应对病毒感染进程的影响。The endoplasmic reticulum is the major site of protein synthesis,folding,modification,and sorting in eukaryotic cells.Accumulating evidence indicates that viral infection often disturbs endoplasmic reticulum homeostasis and leads to endoplasmic reticulum stress(ERS).As a self-protection mechanism,endoplasmic reticulum mounts an unfolded protein response(UPR)to relieve the intracellular stress pressure by decreasing endoplasmic reticulum protein production,enhancing protein-folding capacity and promoting endoplasmic reticulum related protein degradation(ERAD).ERS induced by virus infection can activate host immune response and inflammatory response through UPR,and affect the process of viral infection.In this review,we summarized the relationship between the UPR and the host immune system,focusing on the intersection between viral infection related ERS and inflammatory response.

关 键 词：病毒感染 内质网应激 未折叠蛋白反应 炎症反应 

分 类 号：R392[医药卫生—免疫学]