适度的IL-17信号通路的活化有利于抵抗病原体及组织修复，而持续过度活化的IL-17信号通路则会引起慢性炎症性疾病包括自身免疫病、代谢紊乱等。因此，IL-17信号通路必须受到严格调控。NDR1是一个丝苏氨酸蛋白激酶，属于细胞核Dbf-2相关蛋白家族，参与调控细胞凋亡、细胞周期、中性粒复制等过程，而其在IL-17诱导的炎症反应中的作用尚未有报道。我们发现干扰或敲除NDR1表达明显抑制了IL-17诱导的炎症因子的产生。而NDR1敲除小鼠对IL-17诱导的腹腔炎症反应明显下降，提示NDR1正向调控IL-17诱导的炎症反应。进一步研究发现NDR1 促进了IL-17诱导的MAPK及NF-κB的的活化。我们拟在此基础上深入研究NDR1在IL-17诱导的炎症中的作用及具体分子机制。本项目地完成可进一步丰富NDR1分子的生理病理功能， 并为感染性疾病及自身免疫性疾病的诊断和治疗提供新的靶点。

The appropriate IL-17 signaling activation is benefit for the microbial removing and tissue repair, however persistent and overactive IL-17 signaling will result in development of many human chronic diseases, including autoimmune diseases, metabolic disorders. Thus, the signaling of IL-17 should be under tight control to avoid persistent harmful inflammation. NDR1 is a Ser/Thr kinase which belongs to the NDR family and regulates the apoptosis、cell cycle process、chromosome alignment. However, the roles of NDR1 in IL-17-induced-inflammation have not been reported. We found that silencing or knocking out of NDR1 expression inhibited the IL-17-induced cytokines expression in vitro. IL-17-induced peritoneal inflammation was impaired in NDR1-deficient mice. Furthermore, we found silencing of NDR1 expression inhibited the IL-17 induced the MAPK and NF-κB activation. Further characterization of the function and the mechanism of NDR1 in IL-17-induced inflammatory response is essential for understanding of IL-17 signaling and benefit for developing new targets in certain types of infection and autoimmune diseases.