TRIM35通过靶向IRF7负向调节TLR7和TLR9介导的I型干扰素产生。
TRIM35 negatively regulates TLR7- and TLR9-mediated type I interferon production by targeting IRF7.
作者信息
Wang Yanming, Yan Shanshan, Yang Bo, Wang Yan, Zhou Haiyan, Lian Qiaoshi, Sun Bing
机构信息
School of Life Sciences, University of Science and Technology of China, Hefei, China.
Key Laboratory of Molecular Virology & Immunology, Institute Pasteur of Shanghai, Chinese Academy of Sciences, Shanghai, China.
出版信息
FEBS Lett. 2015 May 22;589(12):1322-30. doi: 10.1016/j.febslet.2015.04.019. Epub 2015 Apr 20.
Toll-like receptor 7 (TLR7) and TLR9 sense viral nucleic acids and induce type I IFN production, which must be properly controlled to avoid autoimmune diseases. Here, we report the negative regulation of TLR7/9-mediated type I IFN production by TRIM35. TRIM35 expression is induced by TLR7/9 stimulation and then interacts with IRF7, which is the master regulator of type I IFN response. Furthermore, TRIM35 promotes the K48-linked ubiquitination of IRF7 and induces its degradation via a proteasome-dependent pathway. Therefore, TRIM35 is a negative feedback regulator of TLR7/9-mediated type I IFN production due to its ability to suppress the stability of IRF7.
Toll样受体7（TLR7）和TLR9可识别病毒核酸并诱导I型干扰素产生，而这一过程必须得到适当控制以避免自身免疫性疾病。在此，我们报告了TRIM35对TLR7/9介导的I型干扰素产生的负调控作用。TRIM35的表达由TLR7/9刺激诱导，随后与I型干扰素反应的主要调节因子IRF7相互作用。此外，TRIM35促进IRF7的K48连接的泛素化，并通过蛋白酶体依赖性途径诱导其降解。因此，由于TRIM35能够抑制IRF7的稳定性，它是TLR7/9介导的I型干扰素产生的负反馈调节因子。
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