报告人简介：

郑春福，福建医科大学特聘教授，博导。加拿大University of Calgary的兼职教授。入选Elsevier 2021/2022年全球Top1%顶尖科学家榜单；在I型单纯疱疹病毒（HSV-1）感染与宿主相互作用的分子机制研究、HSV-1逃逸宿主抗病毒天然免疫研究中取得突破性研究成果，发表SCI论文120余篇，总引用次数5000余次，H-index为38。主持973计划、国家自然科学基金等多项基金，担任多个顶级期刊杂志的编辑和编委。

报告大纲：

TANK-binding kinase 1 (TBK1) is crucial in producingtype Ⅰ interferons (IFN-Ⅰ) that play critical functions in antiviral innateimmunity. The tight regulation of TBK1, especially its activation, is veryimportant. Here we identify NLRC4 as a positive regulator of TBK1. Ectopicexpression of NLRC4 facilitates the activation of the IFN-β promoter, the mRNAlevels of IFN-β, ISG54, and ISG56, and the nuclear translocation of interferonregulatory factor 3 induced by cGAS and STING. Consistently, under herpes simplexvirus-1 (HSV-1) infection, knockdown or knockout of NLRC4 in BJ cells andprimary peritoneal macrophages from Nlrc4-deficient (Nlrc4-/- ) miceshow attenuated Ifn-β, Isg54, and Isg56 mRNA transcription, TBK1phosphorylation, and augmented viral replications. Moreover, Nlrc4-/-mice show higher mortality upon HSV-1 infection. Mechanistically, NLRC4facilitates the interaction between TBK1 and the E3 ubiquitin ligase CBL toenhance the K63-linked polyubiquitination of TBK1. Our study elucidates a previouslyuncharacterized function for NLRC4 in upregulating the cGAS-STING signalingpathway and antiviral innate immunity.