IL-17通过诱导细胞产生炎性和趋化因子，抵抗和清除病原微生物感染、维持机体免疫系统稳态，其信号通路受到严密调控。RKIP属于PEBP家族，主要参与调控细胞分化，细胞周期分布等生物学过程，并促进肿瘤细胞的凋亡，抑制肿瘤转移。RKIP在炎症方面的确切作用未有报道。我们前期研究发现过表达RKIP明显促进IL-17诱导的炎症因子的产生；而干扰RKIP的表达则抑制IL-17诱导的炎症因子产生，提示RKIP正向调控IL-17信号效应。本项目拟在此基础上研究RKIP表达在体内、体外对在IL-17诱导炎症反应的作用及机制；明确RKIP促进IL-17介导的炎症反应调控作用，阐明RKIP调控IL-17信号效应的分子机制，进一步明确RKIP分子的生理、病理功能，揭示IL-17信号转导新机制。本项目的完成可为阐明IL-17诱导的炎症相关的免疫稳态维持和精细调控机制提供理论基础，并为相关疾病防治提供新靶点。

IL-17 has a significant role in driving inflammatory responses to infection of pathogens, allergens, the signaling of IL-17 should be under tight control to avoid persistent harmful inflammation. RKIP play a important role as a master modulator of many pivotal intracellular signaling cascades that control cellular growth, motility, apoptosis, genomic integrity, and therapeutic resistance. However, the understanding of the roles of RKIP in inflammation is poor. Our preliminary research found that RKIP has effect on IL-17 mediated inflammation, and overexpression of RKIP promotes the expression of pro-inflammatory genes such as chemokines, cytokines, downregulation of RKIP inhibits the expression of pro-inflammatory genes. Furthermore, RKIP can enhance the activation of MAPK and NF-κB path- ways induced by IL-17.This proposal will explore the effect and its underlying mechanisms regulating on IL-17 mediated inflammation. The results will helpful to clarify the physiological and pathological function of RKIP. and provide new targets for disease prevention.