Th17被认为是除Th1、Th2之外的第三类效应T细胞，和自身免疫病的发病密切相关，是当今免疫学研究的热点之一。IL-23是Th17细胞分化发育和功能维持过程中的重要因子。IL-23的缺失会显著降低Th17细胞生成，同时可降低模型鼠自身免疫性疾病的发生率、减轻其发病的严重程度。本课题选择IL23p19亚基受体蛋白IL23R为靶分子, 通过基因工程手段，真核转染成功表达融合蛋白rhIL-23R/Fc，通过预实验验证了重组hIL-23R/Fc融合蛋白体外阻止活性异常增高的Th17细胞发育的效能，本课题将进一步利用实验性变态反应性脑脊髓炎（EAE）动物模型，静脉输入融合蛋白rhIL-23R/Fc，观察融合蛋白体内实验的药理学指标，确定治疗自身免疫性疾病模型鼠的效果及分子机制，为银屑病、多发性硬化症、Crohn's病等多种临床免疫性疾病治疗提供重要的实验依据。

Th17 cells, a third subset of CD4+ T effector cells in addition to Th1, Th2, emerge as a hot topic in immunology, and play an important role in autoimmune diseases. IL-23 plays a critical role in maintaining and stabilizing Th17 cells phenotype. The absence of IL-23 can significantly down-regulate the level of Th17 cells, and also can reduce the incidence of EAE. In our project, we constructed a Fc fusion protein with IL23Rp19 subunit to prolong fusion proteins' half-life, we have always analyzed the function of rhIL-23R/Fc with inhibiting Th17 cells polarized in vitro，Furthermore, we want to obtain the pharmacological data of the role of rhIL-23/Fc fusion protein in EAE model，which can indicate the mechanism of rhIL23R/Fc fusion protein in autoimmune disease in mice model, and provide new therapy evidence for autoimmune diseases like psoriasis, multiple sclerosis, Crohn's disease and so on.