8月16日，国际学术期刊《Journal of Immunology》在线发表了中国科学院上海生物化学与细胞生物学研究所孙兵研究组题为“Negative Regulation of Nmi on Virus-Triggered Type I IFN Production by Targeting IRF7”的研究论文。报道了病毒诱导的分子NMI（N-Myc and STATs interactor）可以促进IRF7泛素化，通过蛋白酶体途径降解，从而抑制宿主细胞的抗病毒反应，是一个病毒介导的免疫反应负性调控蛋白。
病毒感染宿主细胞以后，可以诱发抗病毒免疫反应。宿主细胞的模式识别分子RIG-I和MDA-5可以识别胞内的病毒RNA。通过接头分子VISA(也称为MAVS、IPS-1或Cardif)引发下游信号分子信号传递，促进转录因子IRF3/IRF7和NF-kB的激活，进而诱导I型干扰素和炎性因子的产生，其中IRF7是诱导I型干扰素产生的关键性转录因子之一。
孙兵研究组博士生王洁、杨波等发现NMI分子可以负性调控病毒诱导的I型干扰素产生。Sendai virus感染细胞后，NMI分子被诱导表达，NMI可以作用于IRF7并促进IRF7的K48位泛素化以及蛋白酶体途径降解。体外过表达NMI可以抑制IFN-a/b的表达，而下调NMI则促进IFN-a/b的表达。进一步在NMI转基因小鼠身上感染Sendai virus，其肺部的IFN-a/b表达明显降低。
I型干扰素在抗病毒过程中发挥了关键的作用，而它的表达又是受到精细的调控，过度表达将造成机体损害。该研究揭示了一种新的抗病毒反应调控和保持免疫平衡的机制。
该项工作得到了国家科技部、国家基金委的资助。（生物谷Bioon.com）
doi:10.4049/jimmunol.1300740
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Negative Regulation of Nmi on Virus-Triggered Type I IFN Production by Targeting IRF7.
Wang J, Yang B, Hu Y, Zheng Y, Zhou H, Wang Y, Ma Y, Mao K, Yang L, Lin G, Ji Y, Wu X, Sun B.
Viral infection causes host cells to produce type I IFNs, which play a critical role in viral clearance. IFN regulatory factor (IRF) 7 is the master regulator of type I IFN-dependent immune responses. In this article, we report that N-Myc and STATs interactor (Nmi), a Sendai virus-inducible protein, interacted with IRF7 and inhibited virus-triggered type I IFN production. The overexpression of Nmi inhibited the Sendai virus-triggered induction of type I IFNs, whereas the knockdown of Nmi promoted IFN production. Furthermore, the enhanced production of IFNs resulting from Nmi knockdown was sufficient to protect cells from infection by vesicular stomatitis virus. In addition, Nmi was found to promote the K48-linked ubiquitination of IRF7 and the proteasome-dependent degradation of this protein. Finally, an impairment of antiviral responses is also detectable in Nmi-transgenic mice. These findings suggest that Nmi is a negative regulator of the virus-triggered induction of type I IFNs that targets IRF7.
