类风湿性关节炎(RA)是以慢性破坏性关节病变为特征的自身免疫疾病，目前仍无法治愈，因此发掘新的治疗方式有重要意义。本课题组发现齿龈间充质干细胞(GMSC)可以治疗RA，同时GMSC高表达B7-H1。B7-H1是免疫负性调节的重要靶点，那么B7-H1是否介导GMSC功能？机制是什么？我们预实验发现，B7-H1高表达的GMSC免疫抑制功能高于B7-H1低表达的GMSC，阻断B7-H1后GMSC对T细胞增殖及炎症因子分泌的抑制作用降低，同时GMSC上B7-H1发挥功能与STAT3信号相关。据此我们提出假设：B7-H1通过STAT3通路调节GMSC的免疫调控功能从而治疗类风湿性关节炎。本项目拟采用胶原诱导性关节炎小鼠模型，运用流式分选、特异性抑制剂等手段，阐明B7-H1在GMSC治疗类风湿性关节炎中的作用及机制，为寻找功能更强大的GMSC亚群提供科学依据，为进一步治疗类风湿性关节炎提供指导价值。

Rheumatoid arthritis (RA) is a chronic human autoimmune disease characterized by inflammatory synovial joints, progressive destruction of cartilage, bone erosions and ankylosis, new therapeutics are necessary for the reason that RA is cannot be completely cured. We previously found that Gingiva-derived mesenchymal stem cell (GMSC) could ameliorated RA and further studies showed that GMSC highly expressed B7-H1. B7-H1 signaling mediated a crucial role in immune-suppression, so we want to explore whether the B7-H1 pathway mediated the immune regulation of GMSCs and the related mechanism. We found B7-H1-high expressed GMSCs showed higher immune-suppressive effect compared with B7-H1-low expressed GMSCs in vitro, the immunosuppression of GMSC was decreased when the B7-H1 signaling was blocked. Furthermore, we found the regulation of B7-H1 on GMSC was related with STAT3 pathway. Therefore, we hypothesize that B7-H1 plays an important role in the immunoregulation of GMSCs on CIA murine model through STAT3. We plan to use CIA murine model, flow cytometry sorting and specific blocking antibody or inhibitor to systemically expound the significant role and the related mechanisms of B7-H1 signaling on the immune-suppression of GMSCs. The expected results will take a further insight on the more effective GMSC subsets and target for future treatment on RA.