模式识别受体识别病毒核酸诱导产生I型干扰素,在宿主抗病毒固有免疫反应中起关键性作用。尽管在过去10多年中备受关注，病毒核酸模式识别受体介导I型干扰素产生的调节机制仍未完全阐明。我们初步的实验结果提示，Hippo信号通路蛋白激酶NDR1、LATS1可活化GSK3并促进病毒感染诱导的Stat1活化以及IFN-β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NDR1、LATS1表达在体内外对I型干扰素介导的抗病毒固有免疫反应的调节作用，研究NDR1、LATS1是否协同调节GSK3和Stat1的活化及其作用机制，阐明NDR1、LATS1调节抗病毒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。

Type I interferon, induced by activation of Pattern recognition receptors (PRR) which recognize virus nucleic acid, play important roles in antivirus innate immunity. Although intensively studied, the mechanism regulating PRR-mediated interferon production remains unilluminated. Our primary results indicate that expression of Hippo pathway kinases NDR1 and LATS1 positively regulates virus infection-induced IFN-β production possibly by activating GSK3 and Stat1.The present project will confirm the role of NDR1 and LATS1 in type I interferon-mediated antivirus innate immune responses both in vitro and in vivo, illuminate the mechanism by which NDR1 and LATS1 regulate innate immune responses, providing novel target for the therapy of virus infection diseases.