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
蔡依廷 1陈玮1
作者信息
- 1. 浙江大学医学院免疫学研究所,杭州 310058
- 折叠
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.
Abstract
Innate immune response is the first line of immune defense in our body against invaded pathogens.After receive pathogen stimulation,immune cells synthesize abundant type Ⅰ interferons(IFNs)through activating three different signaling path-ways to establish strong antiviral immune response.Mounting evidences have revealed that selective autophagy participates in the regu-lation of innate type Ⅰ IFN 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 autophago-some-lysosome pathway.Therefore,autophagy and E3 ubiquitin ligases integrate the spatiotemporal regulation of innate type Ⅰ IFN response.In this review,we summarized current data elucidating the critical role of autophagy and E3 ubiquitin ligases in the regula-tion of innate immune response.
关键词
泛素化/自噬/固有免疫/Ⅰ型干扰素Key words
Ubiquitination/Autophagy/Innate immunity/Type Ⅰ interferon引用本文复制引用
基金项目
浙江省自然科学基金(LY17C080003)
出版年
2024