Cell Res:武汉大学钟波组在抗病毒天然免疫应答领域取得重要进展

2018-11-13 佚名 病毒学界

2018年11月8日,武汉大学生命科学学院与医学研究院钟波教授作为通讯作者在国际权威期刊Cell Research (IF:15.3) 上在线发表题为“Induction of OTUD4 by viral infection promotes antiviral responses through deubiquitinating and stabilizing MAVS”(病毒感染诱导的OTU

2018年11月8日,武汉大学生命科学学院与医学研究院钟波教授作为通讯作者在国际权威期刊Cell Research (IF:15.3) 上在线发表题为“Induction of OTUD4 by viral infection promotes antiviral responses through deubiquitinating and stabilizing MAVS”(病毒感染诱导的OTUD4通过稳定MAVS的蛋白水平促进抗病毒免疫应答)的学术论文。该文阐述了病毒诱导表达的去泛素化酶OTUD4通过去泛素化并稳定重要信号蛋白MAVS调控天然免疫应答的过程。2016级博士研究生刘雨田子为该论文的第一作者。

天然免疫是保护机体抵御病原微生物的入侵的第一道生理防线。其中MAVS(也称VISA)介导的信号通路在机体抗RNA病毒天然免疫应答的过程中扮演着重要角色,其功能受到多种翻译后修饰的严格调控,包括泛素化和去泛素化,但是之前的研究只报道集中在鉴定泛素化MAVS的E3泛素连接酶,对于MAVS是否存在去泛素化调控及其分子机制与生理学意义尚不清楚。

为了找到调控MAVS去泛素化过程的分子,该课题组筛选了与MAVS相互作用的DUB(去泛素化酶系列)库,并鉴定了一个候选蛋白OTUD4(ovarian tumor family deubiquitinase 4)。发现OUT家族成员中,有且仅有OTUD4与MAVS相互作用,且其表达水平受到病毒感染与IRF3/7的调控。在人细胞系中敲低或在小鼠中敲除OTUD4均抑制病毒感染后IRF3余NF-kB的活化以及I型干扰素与炎性细胞因子的表达,且这一过程依赖于其去泛素化酶活性。OTUD4条件敲除小鼠体对VSV(Vesicular Stomatitis Virus,水疱性口炎病毒)易感,病毒复制增强,血清中I型干扰素等细胞因子的表达水平显着受到抑制。OTUD4被报道具备水解K63以及K48链接泛素链的活性,该研究进一步揭示OTUD4水解K63链接泛素链的活性并非其调控抗病毒天然免疫信号转导所必须,暗示其水解K48链接泛素链的活性参与了该过程的调控。



由于OTUD4与MAVS相互作用,并在MAVS水平调控抗病毒天然免疫信号转导,研究者随后检测了病毒感染前后MAVS K48链接泛素化修饰的情况。结果表明敲除OTUD4促进MAVS上K48链接泛素链的修饰,促进MAVS的降解(上图)。这一过程被蛋白酶体抑制剂MG132所抑制,而不能被自噬途径抑制剂Baf A1抑制,暗示OTUD4通过挽救MAVS的蛋白酶体途径降解进而促进抗病毒天然免疫应答。此外,在OTUD4敲除细胞中回补MAVS而非RIG-I能完全回复病毒感染诱导的I型干扰素等细胞因子的表达,并抑制病毒的复制。这一发现首次揭示了OTUD4通过正反馈途径调控MAVS的去泛素化的机制,提示OTUD4可能是一个抗病毒免疫治疗的潜在靶点。

该项研究依托于武汉大学生命科学学院和武汉大学医学研究院,受到国家重大基础研究计划(973)、国家自然科学基金委青年项目、面上项目、优秀青年科学基金、湖北省自然科学基金以及武汉大学自主科研项目等项目的支持。

原始出处:Tianzi Liuyu, Keying Yu, Liya Ye, et al. Induction of OTUD4 by viral infection promotes antiviral responses through deubiquitinating and stabilizing MAVS. Cell Res. 08 November 2018

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    2019-01-09 维他命
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    2018-11-15 yahu
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