RIG-I-like receptor-induced IRF3 mediated pathway of apoptosis （RIPA）： a new antiviral pathway

作     者：Saurabh Chattopadhyay Ganes C. Sen 

作者机构：Department of Medical Microbiology and Immunology University of Toledo College of Medicine and Life Sciences 3000 Arlington Avenue Mailstop 1021 Toledo OH 43614 USA Cleveland Clinic Department of Immunology 9500 Euclid Avenue NE20 Cleveland OH 44195 USA 

出 版 物：《Protein & Cell》 (蛋白质与细胞（英文版）)

年 卷 期：2017年第8卷第3期

页      面：165-168页

核心收录：

学科分类：07[理学] 08[工学] 

基　　金：supported by the American Heart Association Scientist Development to S.C the National Institutes of Health to G.C.S 

主　　题：RIPA IRF3 innate immunity 

摘      要：The innate immune response is the first line of host defense to eliminate viral infection. Pattern recognition receptors in the cytosol, such as RIG-I-like receptors （RLR） and Nod-like receptors （NLR）, and membrane bound Toll like receptors （TLR） detect viral infection and initiate transcription of a cohort of antiviral genes, including interferon （IFN） and interferon stimulated genes （ISGs）, which ultimately block viral replication. Another mechanism to reduce viral spread is through RIPA, the RLR-induced IRF3-mediated pathway of apoptosis, which causes infected cells to undergo pre- mature death. The transcription factor IRF3 can mediate cellular antiviral responses by both inducing antiviral genes and triggering apoptosis through the activation of RIPA. The mechanism of IRF3 activation in RIPA is dis- tinct from that of transcriptional activation; it requires linear polyubiquitination of specific lysine residues of IRF3. Using RIPA-active, but transcriptionally inactive, IRF3 mutants, it was shown that RIPA can prevent viral replication and pathogenesis in mice.