BCL-6/Blimp-1信号及其表观遗传学因素改变是滤泡辅助性T细胞 (Tfh) 分化的决定性因素，是溃疡性结肠炎(UC)发病的关键因素之一，也是其药物作用机制研究热点，提示干预BCL-6/Blimp-1信号调控Tfh分化可能是治疗UC的的有效策略之一。我们前一个国家基金表明，姜黄素(Cur)有效治疗UC是通过抑制DCs活性恢复免疫平衡实现的，且明显抑制该信号上关键蛋白表达，提示Cur具有调控Tfh分化和BCL-6/Blimp-1信号潜在可能。故我们提出Cur可能通过干预该信号调控Tfh分化治疗UC的科学假设。我们再次验证Cur治疗UC有效性，并评价Tfh分型、Tfh亚群及记忆性Tfh水平，并分析BCL-6/Blimp-1信号上核心指标、正性调控和负性调控因素的表达，继而考察该信号表观遗传学因素的改变，从干预BCL-6/Blimp-1信号调控Tfh分化全面探索Cur治疗UC的作用机制。

In the recent years，abnormal differentiation of follicular helper T cells (Tfh) resulted in inflammatory bowel disease (IBD) is a research hotspot, while BCL-6/Blimp-1 signaling pathway and its epigenetics factors change are the determining factor of Tfh differentiation. And these are critical factors in pathogenesis of ulcerative colitis. All evidences had hinted that it is an effective therapeutic strategy treated IBD via regulating Tfh differentiation by BCL-6/Blimp-1 signaling pathway. In our previous NSFC project, we found that Curcumin (Cur) effectively treated experimental colitis, which was realized by inhibiting Dendritic Cells via repressing JAK/STAT/SOCS to restore immunologic balance, and Cur obviously inhibited expressions of key upstream proteins of BCL-6/Blimp-1 signaling pathway. Our results indicated that Cur have potential functions on regulation of Tfh differentiation and BCL-6/Blimp-1 signaling pathway. So, we proposed scientific hypothesis that Cur effectively treated UC by regulating BCL-6/Blimp-1 pathway to control Tfh differentiation. In the present project, we will verify the effect of Cur treated experimental colitis, and evaluate levels of Tfh types, Tfh subpopulation and memory of Tfh. While we will analyze expressions of core index, positive and negative regulation of BCL-6/Blimp-1 pathway, and observe its epigenetics factors change on histone modification and miRNA. It it to explore mechanism of Cur treated UC via BCL-6/Blimp-1 pathway to regulate Tfh differentiation, and to expand the category of Cur’s immunophamacology.