泛素化参与自噬调节固有免疫应答的研究进展  

Research progress of ubiquitination involved in autophagy in regulating innate immune response

作　　者：蔡依廷 陈玮[1] CAI Yiting;CHEN Wei(Institute of Immunology,Zhejiang University,School of Medicine,Hangzhou 310058,China)

机构地区：[1]浙江大学医学院免疫学研究所,杭州310058

出　　处：《中国免疫学杂志》2024年第7期1525-1535,共11页Chinese Journal of Immunology

基　　金：浙江省自然科学基金(LY17C080003)。

摘　　要：固有免疫应答是人体抵御病原体入侵的第一道防线。接受病原体刺激后,免疫细胞通过3条主要信号通路诱导Ⅰ型干扰素(IFNs)合成,从而建立全面的抗病毒反应。越来越多的证据表明,选择性自噬参与对固有免疫Ⅰ型IFN应答信号的调节,可抑制过度的免疫反应。E3泛素连接酶可催化形成不同类型的多聚泛素链,是自噬调控抗病毒信号转导的关键参与者,协同自噬在时间和空间上对固有免疫信号转导进行调节。本综述总结了自噬调节固有免疫的最新研究成果,并讨论E3泛素连接酶在其中的关键作用。Innate immune response is the first line of immune defense in our body against invaded pathogens.After receive pathogen stimulation,immune cells synthesize abundant typeⅠinterferons(IFNs)through activating three different signaling pathways to establish strong antiviral immune response.Mounting evidences have revealed that selective autophagy participates in the regulation of innate typeⅠIFN response and prevents the excessive activation of immune responses.E3 ubiquitin ligases transfer different type of polyubiquitin chains to some key signaling proteins,and trigger the selective degradation of these proteins through autophagosome-lysosome pathway.Therefore,autophagy and E3 ubiquitin ligases integrate the spatiotemporal regulation of innate typeⅠIFN response.In this review,we summarized current data elucidating the critical role of autophagy and E3 ubiquitin ligases in the regulation of innate immune response.

关 键 词：泛素化 自噬 固有免疫 Ⅰ型干扰素 

分 类 号：R392[医药卫生—免疫学]