树突状细胞（DCs）是启动和调节炎症性肠病(IBD)炎症反应的重要环节。研究发现髓样分化蛋白-1（MD-1）可通过调节DCs的功能影响移植免疫排斥反应。我们前期研究观察到MD-1基因缺失可降低小鼠对葡聚糖硫酸钠（DSS）诱导结肠炎的易感性，伴随着肠黏膜固有层DCs表面成熟分子（MHC-Ⅱ、CD40、CD86）的表达水平降低。因此，我们假设MD-1基因缺失通过调节DCs的功能来抑制结肠炎小鼠的肠道炎症。为此，以野生型C57BL/6J和MD-1-/-C57BL/6J小鼠建立DSS诱导的结肠炎模型：（1）体内、体外观察MD-1基因缺失对结肠炎小鼠肠道DCs功能的影响；（2）过继转移MD-1基因缺失的DCs至DSS诱导的结肠炎小鼠体内，观察其对肠道炎症的影响。本项目旨在明确MD-1基因缺失抑制结肠炎小鼠肠道炎症是通过调节DCs的功能实现的，并为寻找IBD治疗的新靶点提供理论依据。

Dendritic cells (DCs) play an important role in initiating and modulating immune responses in inflammatory bowel disease (IBD). Myeloid differentiation 1(MD-1) was shown to affect immunosuppression of the immunologic rejection through regulating the function of DCs. Our previous study found that MD-1 deficiency attenuates DSS induced colitis in mice, accompanied by decreased expression of maturation markers of DCs, such as MHC-Ⅱ、CD40、CD86. Thus, it was hypothesized that MD-1 deficiency prevents intestinal inflammation through modulating the function of DCs in experimental colitis mice. Therefore, we use wild type C57BL/6J mice and MD-1-/- C57BL/6J mice to establish a mouse mode of DSS-induced colitis: (1) To investigate the effect of MD-1 deficiency on the function of DCs in experimental colitis mice in vivo and ex in vitro. (2) To investigate intestinal inflammation via adoptive transfer of MD-1-/- DCs into wild type mice following DSS-induced colitis. Our study will provided a novel mechanism that MD-1 deficiency has a protective effect on DSS-induced colitis by modulating the function of intestinal DCs, thereby suggesting that MD-1 might be a target for future interventional therapies of IBD.