免疫球蛋白IgG与肠道巨噬细胞活化型FcγR结合可诱导Th17细胞免疫，是引发溃疡性结肠炎（UC）的关键环节之一。申请人前期研究结果表明，艾灸能抑制UC大鼠外周血促炎症因子IL-1β蛋白浓度。本课题在艾灸治疗UC有效的基础上，从IgG-FcγR途径与NLRP3炎症小体相互作用的角度，应用免疫组化、实时定量PCR、流式细胞等分子生物学技术和方法，结合基因敲除小鼠验证：①拟阐明UC的发生与IgG和巨噬细胞活化型FcγR相关，艾灸能抑制IgG-FcγR途径，减轻结肠黏膜炎症反应；②阐释IgG与肠道巨噬细胞活化型FcγR结合，能介导巨噬细胞NLRP3-IL-1β的级联反应，诱导UC病变部位Th17细胞释放促炎症因子，及艾灸调节效应；③明确艾灸可能通过抑制肠道巨噬细胞IgG-FcγR途径，抑制NLRP3炎症小体的活化，减轻UC结肠黏膜炎症，以达艾灸治疗UC之目的，为临床推广应用提供实验依据。

The binding of immunoglobulin IgG and activated FcγR on intestinal macrophage can induce Th17 cell immunity, which is one of the key links leading to ulcerative colitis (UC). Previous results of the applicant showed that moxibustion could inhibit the concentration of proinflammatory factor IL-1β protein in peripheral blood of UC rats. Based on the effectiveness of moxibustion in the treatment of UC, from the perspective of interaction between the IgG-FcγR and NLRP3 inflammasome this study applies modern molecular biology techniques and methods such as immunohistochemistry, real-time quantitative PCR, flow cytometry, and combined with gene knockout mice: ①to clarify that UC is related to IgG and activated FcγR on macrophage, moxibustion can inhibit the IgG-FcγR pathway and reduce colon inflammation; ②to explain that IgG binds to activated FcγR on intestinal macrophage and can mediate the cascade reaction of NLRP3-IL-1β in macrophages, induce the release of pro-inflammatory factors from Th17 cells in UC lesions, as well as the regulating effect of moxibustion;③to clarify that moxibustion may inhibit the activation of NLRP3 inflammasome by inhibiting the IgG-FcγR pathway of intestinal macrophages, then reduce the UC intestinal mucosal inflammation to achieve the purpose of moxibustion treatment of UC, so as to provide experimental basis for clinical promotion and application.