NLRP11 破坏 MAVS 信号复合物以抑制 I 型干扰素信号和病毒诱导的细胞凋亡。
NLRP11 disrupts MAVS signalosome to inhibit type I interferon signaling and virus-induced apoptosis.
机构信息
Key Laboratory of Gene Engineering of the Ministry of Education, State Key Laboratory of Biocontrol, School of Life Sciences, Sun Yat-sen University, Guangzhou, China.
School of Life Sciences, Zhengzhou University, Zhengzhou, Henan, China.
出版信息
EMBO Rep. 2017 Dec;18(12):2160-2171. doi: 10.15252/embr.201744480. Epub 2017 Nov 2.
Abstract
MAVS signalosome plays an important role in RIG-I-like receptor (RLR)-induced antiviral signaling. Upon the recognition of viral RNAs, RLRs activate MAVS, which further recruits TRAF6 and other signaling proteins to initiate type I interferon (IFN) activation. MAVS signalosome also regulates virus-induced apoptosis to limit viral replication. However, the mechanisms that control the activity of MAVS signalosome are still poorly defined. Here, we report NLRP11, a Nod-like receptor, is induced by type I IFN and translocates to mitochondria to interact with MAVS upon viral infection. Using MAVS as a platform, NLRP11 degrades TRAF6 to attenuate the production of type I IFNs as well as virus-induced apoptosis. Our findings reveal the regulatory role of NLRP11 in antiviral immunity by disrupting MAVS signalosome.
摘要
MAVS 信号转导体在 RIG-I 样受体 (RLR) 诱导的抗病毒信号转导中发挥重要作用。在识别病毒 RNA 后，RLR 激活 MAVS，MAVS 进一步招募 TRAF6 和其他信号蛋白启动 I 型干扰素 (IFN) 的激活。MAVS 信号转导体还调节病毒诱导的细胞凋亡以限制病毒复制。然而，控制 MAVS 信号转导体活性的机制仍知之甚少。在这里，我们报告了 NOD 样受体 NLRP11，它被 I 型 IFN 诱导，并在病毒感染时易位到线粒体与 MAVS 相互作用。NLRP11 作为一个平台，可降解 TRAF6 以减少 I 型 IFN 的产生和病毒诱导的细胞凋亡。我们的研究结果揭示了 NLRP11 通过破坏 MAVS 信号转导体在抗病毒免疫中的调节作用。
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