期刊
JOURNAL OF IMMUNOLOGY
卷 187, 期 12, 页码 6456-6462出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.1003691
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资金
- Chinese Academy of Sciences [KSCX2-YW-R-161, KSCX2-YW-R-169, KSCX2-EW-J-14]
- National Ministry of Science and Technology [2007DFC31700]
- National Natural Science Foundation of China [30950002, 30623003, 30721065, 30801011, 30870126, 31030029, 90713044]
- National Science and Technology Major Project [2009ZX10004-016, 2008ZX10004-002, 2009ZX10004-105]
- National 973 Key Project [2007CB512404]
- Shanghai Pasteur Health Research Foundation [SPHRF2008001, SPHRF2009001]
- National 863 Project [2006AA02A247]
- Li Kha Shing Foundation
- Tsinghua-Yu Yuan Foundation [20200584]
- Janssen Investigator award
- Tsinghua University [985]
IRF7 is known as the master regulator in virus-triggered induction of type I IFNs (IFN-I). In this study, we identify GBP4 virus-induced protein interacting with IRF7 as a negative regulator for IFN-I response. Overexpression of GBP4 inhibits virus-triggered activation of IRF7-dependent signaling, but has no effect on NF-kappa B signaling, whereas the knockdown of GBP4 has opposite effects. Furthermore, the supernatant from Sendai virus-infected cells in which GBP4 have been silenced inhibits the replication of vesicular stomatitis virus more efficiently. Competitive coimmunoprecipitation experiments indicate that overexpression of GBP4 disrupts the interactions between TRAF6 and IRF7, resulting in impaired TRAF6-mediated IRF7 ubiquitination. Our results suggest that GBP4 is a negative regulator of virus-triggered IFN-I production, and it is identified as a novel protein targeting IRF7 and inhibiting its function. The Journal of Immunology, 2011, 187: 6456-6462.
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