SRA Suppresses Antiviral Innate Immune Response in Macrophages by Limiting TBK1 K63 Ubiquitination via Deubiquitinase USP15

Author:

Li Lei1ORCID,Luo Jialiang12,Zhu Zhengyumeng1,Xu Qishan1,Wang Ping13,Chang Bo2,Wang Di4,Yu Lu1,Lu Xiao2,Zhou Jia2,Zuo Daming15ORCID,Chen Qingyun3

Affiliation:

1. Department of Medical Laboratory, Guangdong Province Key Laboratory of Immune Regulation and Immunotherapy, School of Laboratory Medicine and Biotechnology, Southern Medical University, Guangzhou, Guangdong, P.R. China

2. Department of Immunology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, Guangdong, P.R. China

3. Medical Research Institute, Guangdong Provincial People’s Hospital, Guangdong Academy of Medical Sciences, Guangzhou, Guangdong, P.R. China

4. Department of Dermatology, Dermatology Hospital of Southern Medical University, Southern Medical University, Guangzhou, Guangdong, P.R. China

5. Microbiome Medicine Center, Department of Laboratory Medicine, Zhujiang Hospital, Southern Medical University, Guangzhou, Guangdong, P.R. China

Abstract

During virus infection, PRRs are engaged to detect specific viral components, such as viral RNA or DNA, and regulate the innate immune response in the infected cells or other immune cells. We reported that deficiency of SRA, an important innate PRR, promoted IRF3 activation, type I IFN production, and innate antiviral responses against RNA and DNA viruses in vivo and in vitro .

Funder

National Natural Science Foundation of China

GDSTC | Science and Technology Planning Project of Guangzhou

Natural Science Foundation of Guangdong Province

Publisher

American Society for Microbiology

Subject

Infectious Diseases,Cell Biology,Microbiology (medical),Genetics,General Immunology and Microbiology,Ecology,Physiology

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