TLRs和RIG-I是机体识别RNA病毒，激发抗病毒效应的两种主要模式识别受体，尤其是对于RIG-I信号的研究也就是10年不到时间，其信号通路的正向或者负向调控报道还不是很多。IRG-1是一类免疫相关基因，我们先前的研究表明IRG-1在LPS刺激后能够上调，并且在内毒素耐受中发挥重要功能，但IRG-1在机体抗病毒天然免疫中的功能还未有研究。预实验结果表明，IRG-1缺陷的巨噬细胞在RNA病毒VSV感染下产生I型干扰素的能力明显下降，同时病毒的复制明显增强，提示IRG-1具有促进RIG-I信号通路抗病毒效应的作用。本项目拟在预实验基础上，通过体内外感染模型，结合免疫共沉淀、质谱和免疫印记等分子生物学技术手段，进一步探索IRG-1调控RIG-I信号通路的效应和分子机制，丰富机体抗RNA病毒天然免疫应答的调控机制，并为临床干预机体抗病毒效应提供潜在靶点和理论支持。

TLRs and RIG-I are two kinds of pattern recognition receptors for RNA virus. The discovery of RIG-I receptor and its downstream signal transduction has not been more than 10 years, and there are little reports about the regulation of RIG-I signal pathway. We have reported that Immune responsive gene 1(IRG1) can be induced in septic patitents, and play roles in the LPS tolerance. However, whether IRG1 take any role in host anti-viral innate immunity remains unknown. Preliminary experiments revealed that depletion of IRG1 reduced VSV induced IRF3 activation and production of type I interferon, leading to increased virus replication. These results indicate that IRG1 play protective role in anti-virus immunity. In this study, we set to look into the detail about how IRG1 take part in host anti-virus immunity, and the molecule mechanism.