共查询到20条相似文献,搜索用时 31 毫秒
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Thogoto virus ML protein suppresses IRF3 function 总被引:4,自引:0,他引:4
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Porcine reproductive and respiratory syndrome (PRRS) is an emerged disease of swine characterized by negligible response of type I IFNs and viral persistence. We show that the PRRSV non-structural protein 1 (Nsp1) is the viral component responsible for modulation of IFN response. Nsp1 blocked dsRNA-induced IRF3 and IFN promoter activities. Nsp1 did not block phosphorylation and nuclear translocation of IRF3 but inhibited IRF3 association with CREB-binding protein (CBP) in the nucleus. While IRF3 was stable, CBP was degraded, and CBP degradation was proteasome-dependent, suggesting that CBP degradation is not due to the protease activity of Nsp1 but an intermediary is involved. Our data suggest that the Nsp1-mediated CBP degradation inhibits the recruitment of CBP for enhanceosome assembly, leading to the block of IFN response. CBP degradation is a novel strategy for viral evasion from the host response, and Nsp1 may form a new class of viral antagonists for IFN modulation. 相似文献
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Activities of IRF-1. 总被引:3,自引:0,他引:3
Andrea Kr?ger Mario K?ster Katharina Schroeder Hansj?rg Hauser Peter P Mueller 《Journal of interferon & cytokine research》2002,22(1):5-14
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Control of IRF-3 activation by phosphorylation. 总被引:2,自引:0,他引:2
Mitsutoshi Yoneyama Wakako Suhara Takashi Fujita 《Journal of interferon & cytokine research》2002,22(1):73-76
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Eomesodermin promotes interferon‐γ expression and binds to multiple conserved noncoding sequences across the Ifng locus in mouse thymoma cell lines
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Natsuki Fukuoka Misuzu Harada Ai Nishida Yuko Ito Hideki Shiota Takao Kataoka 《Genes to cells : devoted to molecular & cellular mechanisms》2016,21(2):146-162
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Christian Steinberg Katharina Eisencher Olaf Gross Wolfgang Reindl Frank Schmitz Jürgen Ruland Anne Krug 《European journal of immunology》2009,39(4):1007-1018
IFN regulatory factor 7 (IRF7) has been described as the master regulator of type I IFN responses and has been shown to be critical for innate antiviral immunity in vivo. In addition to type I IFN, NK cell responses are involved in the control of viral replication during acute viral infection. To investigate the role of IRF7 in the context of a viral infection that induces a strong NK cell response, the murine cytomegalovirus (MCMV) infection model was used. WT, IRF7‐deficient and IRF3/IRF7‐double deficient mice were infected with MCMV. The systemic IFN‐α response to MCMV was entirely dependent on IRF7, but independent of IRF3. However, peak IFN‐β production during MCMV infection was not affected by the lack of IRF7 or both IRF7 and IRF3. Despite the complete lack of IFN‐α production IRF7‐ and IRF3/IRF7‐deficient mice were surprisingly efficient in controlling MCMV replication and were only modestly more susceptible to MCMV infection than WT mice. NK cell cytotoxicity was unimpaired and NK cell IFN‐γ production was enhanced in IRF7‐deficient mice correlating with increased levels of bioactive IL‐12. Owing to these compensatory mechanisms IRF7‐dependent antiviral immune responses were not essential for resistance against acute MCMV infection in vivo. 相似文献