标题:Mint3 potentiates TLR3/4-and RIG-I-induced IFN-beta expression and antiviral immune responses
作者:Huai, Wanwan; Song, Hui; Yu, Zhongxia; Wang, Wenwen; Han, Lihui; Sakamoto, Takeharu; Seiki, Motoharu; Zhang, Lining; Zhang, Qunye; Z 更多
作者机构:[Huai, Wanwan; Song, Hui; Yu, Zhongxia; Wang, Wenwen; Han, Lihui; Zhang, Lining; Zhao, Wei] Shandong Univ, Sch Med, Dept Immunol, Jinan 250012, Shando 更多
通讯作者:Zhao, W;Zhao, W
通讯作者地址:[Zhao, W]Shandong Univ, Sch Med, Dept Immunol, Jinan 250012, Shandong, Peoples R China;[Zhao, W]Shandong Univ, Sch Med, Key Lab Infect & Immun Shandon 更多
来源:PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
出版年:2016
卷:113
期:42
页码:11925-11930
DOI:10.1073/pnas.1601556113
关键词:interferon; viral infection; TLR; RIG-I; TRAF3
摘要:Type I IFNs (IFN-alpha/beta) play crucial roles in the elimination of invading viruses. Multiple immune cells including macrophages recognize viral infection through a variety of pattern recognition receptors, such as Toll-like receptors (TLRs) and retinoic acid-inducible gene-I (RIG-I)-like receptors, and initiate type I IFN secretion and subsequent antiviral immune responses. However, the mechanisms by which host immune cells can produce adequate amounts of type I IFNs and then eliminate viruses effectively remain to be further elucidated. In the present study, we show that munc18-1-interacting protein 3 (Mint3) expression can be markedly induced during viral infection in macrophages. Mint3 enhances TLR3/4- and RIG-I-induced IRF3 activation and IFN-beta production by promoting K63-linked polyubiquitination of TNF receptor-associated factor 3 (TRAF3). Consistently, Mint3 deficiency greatly attenuated antiviral immune responses and increased viral replication. Therefore, we have identified Mint3 as a physiological positive regulator of TLR3/4 and RIG-I-induced IFN-beta production and have outlined a feedback mechanism for the control of antiviral immune responses.
收录类别:SCOPUS;SCIE
WOS核心被引频次:4
Scopus被引频次:3
资源类型:期刊论文
原文链接:https://www.scopus.com/inward/record.uri?eid=2-s2.0-84991704907&doi=10.1073%2fpnas.1601556113&partnerID=40&md5=c1db6d4146ed09a8550a8cbc1b5bfdd4
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