Negative Regulation of Nmi on Virus-Triggered Type I IFN Production by Targeting IRF7

被引：57

作者：

Wang, Jie ^{[1
]}

Yang, Bo ^{[2
]}

Hu, Yu ^{[1
]}

Zheng, Yuhan ^{[1
]}

Zhou, Haiyan ^{[1
]}

Wang, Yanming ^{[2
]}

Ma, Yonglei ^{[3
]}

Mao, Kairui ^{[1
]}

Yang, Leilei ^{[3
]}

Lin, Guomei ^{[1
]}

Ji, Yongyong ^{[1
]}

Wu, Xiaodong ^{[1
]}

Sun, Bing ^{[1
,2
,3
]}

机构：

[1] Chinese Acad Sci, State Key Lab Cell Biol, Inst Biochem & Cell Biol, Shanghai Inst Biol Sci, Shanghai 200031, Peoples R China

[2] Univ Sci & Technol China, Sch Life Sci, Hefei 230026, Anhui, Peoples R China

[3] Chinese Acad Sci, Mol Virus Unit, Key Lab Mol Virol & Immunol, Inst Pasteur Shanghai, Shanghai 200025, Peoples R China

来源：

JOURNAL OF IMMUNOLOGY | 2013年 / 191卷 / 06期

基金：

中国国家自然科学基金;

关键词：

INTERACTING PROTEIN NMI; NF-KAPPA-B; ANTIVIRAL RESPONSE; TRANSCRIPTION FACTOR; ADAPTER PROTEIN; INTERFERON; MYC; PATHWAY; IFP35; TRAF3;

D O I：

10.4049/jimmunol.1300740

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Viral infection causes host cells to produce type I IFNs, which play a critical role in viral clearance. IFN regulatory factor (IRF) 7 is the master regulator of type I IFN-dependent immune responses. In this article, we report that N-Myc and STATs interactor (Nmi), a Sendai virus-inducible protein, interacted with IRF7 and inhibited virus-triggered type I IFN production. The overexpression of Nmi inhibited the Sendai virus-triggered induction of type I IFNs, whereas the knockdown of Nmi promoted IFN production. Furthermore, the enhanced production of IFNs resulting from Nmi knockdown was sufficient to protect cells from infection by vesicular stomatitis virus. In addition, Nmi was found to promote the K48-linked ubiquitination of IRF7 and the proteasome-dependent degradation of this protein. Finally, an impairment of antiviral responses is also detectable in Nmi-transgenic mice. These findings suggest that Nmi is a negative regulator of the virus-triggered induction of type I IFNs that targets IRF7.

引用

页码：3393 / 3399

页数：7

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