滤泡辅助性T淋巴细胞（Tfh）异常分化在类风湿关节炎（RA）中具有关键作用，寻找抑制Tfh细胞分化的关键因子成为治疗RA的研究焦点。STAT3/Bcl6通路参与Tfh细胞的分化调控，但具体机制仍未充分阐明。有报道称苗药金骨莲可用于RA的治疗。我们前期研究发现，金骨莲通过抑制Tfh细胞的分化进而缓解RA进程。同时，在体外实验中证实该药物对PARP1的活性有抑制作用。PARP1作为STAT3的调节因子，可以激活STAT3/Bcl6进而促进RA中Tfh细胞的分化。基于以上结果，本课题拟从临床、动物、细胞、分子等多层面，采用基因过表达，基因敲降及回复实验干预PARP1及STAT3/Bcl6通路，结合生物信息学分析，深入探讨金骨莲调控PARP1影响STAT3/Bcl6通路从而抑制RA中Tfh细胞分化的具体环节和作用机制，加深RA中Tfh细胞分化作用的认识，为RA的临床治疗提供新线索和新思路。

T-follicular helper (TFH) cells differentiation is responsible for the development of rheumatoid arthritis (RA). Therefore, the critical molecular which enhances Tfh differentiation should be investigated to control RA. STAT3/Bcl6 pathway is critical for Tfh cell differentiation, but the detail underlying mechanism has not been elucidated. Accumulating evidence indicates that Jing Gulian, a traditional Chinese herbal, provided a potential agent for RA. Our recent study indicated that Jing Gulian alleviated the collagen II induced arthritis through inhibiting Tfh differentiation. In vitro assay revealed that Jing Gulian could directly inhibit PARP1 enzyme activity. In addition, PARP1 can promote Tfh cell differentiation via STAT3/Bcl6 pathway in RA. Hence, we intend to investigate the detail mechanism of Jing Gulian regulates Tfh cell differentiation via up- and down- regulated gene expression of PARP1/STAT3/Bcl6 pathway and related rescue assay in vitro, in vivo and in silico respectively. The findings of this study should elucidate the understanding of Tfh cell differentiation in RA, provide a novel therapeutic strategy to control RA and add the experimental evidence for the development of related drugs for RA.