白细胞介素6受体(IL6R)以膜受体和可溶性受体两种形式存在。P28,白细胞介素27的亚基之一，报道能与IL6R结合的蛋白，与sIL6R结合后可以抑制IL6信号通路。目前关于两者在病毒感染过程中所发挥作用的研究报道还很少。本课题以A型流感病毒（IAV）感染引起的免疫应答作为主要研究模型，将阐明sIL6R与p28的复合物在抗病毒天然免疫中的机制作为研究重点。研究内容包括：从细胞、分子以及动物模型水平研究IAV感染过程中对sIL6R及p28的表达变化规律；从转录水平研究IAV感染诱导sIL6R及p28表达的分子机制；sIL6R与p28复合物对IAV复制影响的相关研究及对干扰素通路调节的具体作用机制。通过多种实验技术和手段，阐明p28依赖的sIL6R在宿主抗病毒天然免疫应答中的作用机制。为抗病毒新药物研发打下基础。

The interleukin-6 receptor, which exists as membrane-bound and soluble forms, plays a critical role in the immune response. P28, one of the interleukin-27 subunit, was reported to be associated with IL6R. The combination of p28 with sIL6R can lead to inhibition of IL-6 signaling. Up to date, little is known about the role of sIL6R-p28 complex during viral infections. In this project, we will investigate cellular signaling events which are initiated by Influenza A virus (IAV) infection and define the role of sIL6R and p28 complex in host antiviral innate immune response. The aims of this research project includes: 1，Investigate the kinetic expression of IAV induced sIL6R and p28 in human lung epithelium cell lines, primary cells as well as in animal model. 2, Explore the mechanisms behind sIL6R and p28 expression induced by IAV infection at transcriptional level. 3, The effect of sIL6R and p28 fusion protein on IAV replication and infection. 4, The regulation mechanism of sIL6R and p28 fusion protein on interferon production and related cellular signaling events. Our study will provide new theoretical insight into the development of candidate antiviral drug and elucidate the role of p28-dependent sIL6R in host antiviral immune response by applying different approaches.