Negative Regulation of Nmi on Virus-Triggered Type I IFN Production by Targeting IRF7
| Autor: | Yongyong Ji, Yuhan Zheng, Jie Wang, Yu Hu, Bo Yang, Yonglei Ma, Yanming Wang, Bing Sun, Kairui Mao, Leilei Yang, Haiyan Zhou, Xiaodong Wu, Guomei Lin |
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| Rok vydání: | 2013 |
| Předmět: |
TRAF3
Interferon Regulatory Factor-7 viruses Immunoblotting Immunology Enzyme-Linked Immunosorbent Assay Mice Transgenic Real-Time Polymerase Chain Reaction Transfection Respirovirus Infections Sendai virus Virus Mice Immune system Interferon medicine Animals Humans Immunoprecipitation Immunology and Allergy Gene knockdown biology Reverse Transcriptase Polymerase Chain Reaction Intracellular Signaling Peptides and Proteins NFKB1 biology.organism_classification Mice Inbred C57BL HEK293 Cells Vesicular stomatitis virus Interferon Type I Cancer research IRF7 medicine.drug |
| Zdroj: | The Journal of Immunology. 191:3393-3399 |
| ISSN: | 1550-6606 0022-1767 |
| DOI: | 10.4049/jimmunol.1300740 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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