肠黏膜免疫应答异常是IBD发生的关键因素。肠道树突状细胞(DCs)是最重要的固有免疫细胞，通过活化、迁移和抗原递呈功能，激活适应性免疫反应，引发肠道炎症。新近发现，TL1A作为固有免疫和适应性免疫的连接桥梁，参与IBD发病。既往研究多集中于TL1A对适应性免疫的影响，而对固有免疫的调控作用鲜有研究。我们前期研究发现，髓系高表达TL1A转基因小鼠有自发性肠炎发生，预实验亦提示TL1A可增强BMDCs的抗原递呈功能。本研究采用髓系高表达TL1A转基因小鼠和具有相同遗传背景的野生型小鼠，建立DSS慢性结肠炎模型，同时分离小鼠肠道及骨髓来源的DCs，应用TL1A作为刺激条件，并给予抗TL1A抗体或BAY11-7082阻断NF-κB通路，从体内、外两方面，探讨TL1A对DCs活化、迁移及抗原递呈功能的影响，以及NF-κB信号通路的调控作用，以期为揭示IBD发病机制和临床靶向免疫治疗提供新靶点。

Abnormal immune responses (innate immune and adaptive immune) in intestinal mucosa plays a key role in the pathogenesis of inflammatory bowel disease (IBD). Intestinal dendritic cells (DCs), one of the most important innate immune cells, activate the adaptive immune response through the activation, migration and antigen presentation, leading to prolonged gut inflammation. Recently, TL1A, as the bridge of innate immune and adaptive immune, is associated with the etiology and pathogenesis of IBD. Early studies have focused on the influence of TL1A in adaptive immune. However, the consequences of the innate effects of TL1A have yet to be addressed. We have found FMS-TL1A-GFP-transgenic mice had spontaneous enteritis. Moreover, in our preliminary experiments, TL1A can enhance antigen presentation function of bone marrow derived dendritic cells (BMDCs). In this study, we generated FMS-TL1A-GFP-transgenic and wild-type mice and intestine DCs and BMDCs were isolated. DSS-induced chronic colitis model was established in the laboratory to determine how TL1A regulate activation, migration and the antigen presented function of DCs in vivo and in vitro. In addition, this work will determine the regulation role of NF-κB signaling pathway with TL1A antibodies or BAY 11-7082 (NF-κB pathway blocker), and provide important therapeutic revenue for treatment of IBD.