4月28日，美国《国家科学院院刊》(Proceedings of the National Academy of Sciences of the United States of America, 简称PNAS)发表了武汉大学生命科学学院舒红兵研究组关于细胞抗病毒天然免疫负反馈调控机制的最新研究成果，论文题目是“ISG56 is a negative-feedback regulator of virus-triggered signaling and cellular antiviral response”。该文的第一作者是舒红兵教授的研究生李颖，论文中蛋白质谱鉴定工作是其与中国科学院生物物理所杨福全研究组合作完成的。
天然免疫是细胞和机体天然存在的非特异性或广谱的抗病原微生物的功能，是机体抵抗病原微生物的第一道防线。抗病毒天然免疫最重要的方式之一是通过I型干扰素（α/β干扰素）来介导的。在过去几年中，舒红兵研究组发现了病毒感染诱导I型干扰素表达的信号转导中两个关键的接头蛋白VISA和MITA，论文分别在Molecular Cell和Immunity发表后，引起广泛关注，其中发表在Molecular Cell的论文在发表后三年多时间里已被SCI他引270多次。舒红兵研究组在近年中还发现了多种抗病毒天然免疫信号转导的负调控机制，相关结果发表在Immunity, PNAS, EMBO J.等杂志。
在这项最新研究中，舒红兵研究组发现病毒感染诱导的一个主要细胞蛋白ISG56通过打断MITA相关信号转导复合物的形成，抑制病毒诱导的I型干扰素表达，从而揭示了一种新的抗病毒天然免疫信号转导负反馈调控机制。该项研究扩展了对ISG56功能机理的传统认识，为了解抗病毒天然免疫的精细调控机制提供了新信息。（生物谷Bioon.com）
生物谷推荐原始出处：
PNAS April 28, 2009, doi: 10.1073/pnas.0900818106
ISG56 is a negative-feedback regulator of virus-triggered signaling and cellular antiviral response
Ying Lia, Chao Lia, Peng Xueb, Bo Zhonga, Ai-Ping Maoa, Yong Rana, He Chena, Yan-Yi Wanga, Fuquan Yangb and Hong-Bing Shua,1
IFN-stimulated gene 56 (ISG56) is one of the first identified proteins induced by viruses and type I IFNs. In this study, we identified ISG56 as a virus-induced protein associated with MITA, an adapter protein involved in virus-triggered induction of type I IFNs. Overexpression of ISG56 inhibited Sendai virus-triggered activation of IRF3, NF-κB, and the IFN-β promoter, whereas knockdown of ISG56 had opposite effects. Consistently, overexpression of ISG56 reversed cytoplasmic poly(I:C)-induced inhibition of vesicular stomatitis virus (VSV) replication, whereas knockdown of ISG56 inhibited VSV replication. Competitive coimmunoprecipitation experiments indicated that ISG56 disrupted the interactions between MITA and VISA or TBK1, two components in the virus-triggered IFN signaling pathways. These results suggest that ISG56 is a mediator of negative-feedback regulation of virus-triggered induction of type I IFNs and cellular antiviral responses.
