RIG-I样受体识别病毒RNA，介导炎症因子与I型干扰素产生，是哺乳类动物免疫细胞启动抗病毒固有免疫反应的关键性分子。尽管在过去10年中备受关注，RLR信号转导与调节的分子机制，特别是对炎症与I型干扰素信号免疫平衡的调节机制仍未完全阐明。我们初步的实验结果显示，芳烃受体Ahr表达抑制VSV感染诱导的炎症因子产生同时却增强I型干扰素的产生。本课题将利用基因转染、RNA干扰、基因敲除等方法进一步研究Ahr表达在体内外对RLR介导的固有免疫反应的调节作用，阐明Ahr调节RLR介导的固有免疫反应的分子机制，为感染性疾病的治疗提供新的靶标。

RIG-I-like receptors recognize virus-derived RNA and initiate innate immunity, and thus play important roles in infection diseases. Although intensively studied, the mechanism of PRR signal transduction remains un-illuminated. Our primary results indicate that expression of aryl hydrocarbon receptor, Ahr, oppositely regulates VSV-induced proinflammatory cytokine and type I interferon production. The present project will investigate the role of Ahr in RLR-mediated innate immune responses in vitro and in vivo, illuminate the mechanism by which Ahr regulates innate immune responses, providing novel target for the therapy of infection diseases.