The zinc-finger protein ZFYVE1 modulates TLR3-mediated signaling by facilitating TLR3 ligand binding

作     者：Xuan Zhong Lu Feng Wen-Hua Xu Xin Wu Yi-Di Ding Yan Zhou Cao-Qi Lei Hong-Bing Shu 

作者机构：College of Life SciencesWuhan UniversityWuhan 430072China Department of Infectious DiseasesZhongnan Hospital of Wuhan UniversityWuhan UniversityWuhan 430072China Medical Research InstituteWuhan UniversityWuhan 430072China 

出 版 物：《Cellular & Molecular Immunology》 (中国免疫学杂志（英文版）)

年 卷 期：2020年第17卷第7期

页      面：741-752页

核心收录：

学科分类：1001[医学-基础医学(可授医学、理学学位)] 100102[医学-免疫学] 10[医学] 

基　　金：This work was supported by grants from the State Key R&D Program of China(2017YFA0505800,2016YFA0502102 and 2018YFA0800700) the National Natural Science Foundation of China(31830024,31630045,31870870,31800728,31771555,and 31671418) the China Postdoctoral Science Foundation(2017M620334) the Fundamental Research Funds for the Central Universities(2042019kf0204) the Natural Science Foundation of Hubei Province(2018CFA016) 

主　　题：TLR3 ZFYVE1 ligand binding immune response 

摘      要：Recognition of viral dsRNA by Toll-like receptor 3(TLR3)leads to the induction of downstream antiviral effectors and the innate antiviral immune ***,we identified the zinc-finger FYVE domain-containing protein ZFYVE1,a guanylate-binding protein(GBP),as a positive regulator of TLR3-mediated *** of ZFYVE1 promoted the transcription of downstream antiviral genes upon stimulation with the synthetic TLR3 ligand poly(I:C).Conversely,ZFYVE1 deficiency had the opposite ***1^(−/−) mice were less susceptible than wild-type mice to inflammatory death induced by poly(I:C)but not ***1 was associated with TLR3,and the FYVE domain of ZFYVE1 and the ectodomain of TLR3 were shown to be responsible for their ***1 was bound to poly(I:C)and increased the binding affinity of TLR3 to poly(I:C).These findings suggest that ZFYVE1 plays an important role in the TLR3-mediated innate immune and inflammatory responses by promoting the ligand binding of TLR3.