原因不明复发性流产（URSA）与母胎免疫调节失衡有关。树状细胞（DC）参与了母胎免疫调节，但具体机制尚不明确。我们前期研究发现：在移植物抗宿主病模型中，DC在脾脏及淋巴结内向T细胞进行抗原提呈并引起T细胞增殖，增殖后的T细胞向靶器官游走并攻击靶器官造成损害。在此基础上，本课题拟应用小鼠经典自然流产模型，通过注射CD40单抗及CD40L单抗的方法，观察正常妊娠时、流产时、干预CD40/CD40L协同刺激信号时的母体脾脏及淋巴结内DC的分子表达及抗原提呈功能：即是否与T细胞结合成簇并引起T细胞增殖，增殖后的T细胞是否向母胎界面处游走等情况，与前期成果进行对比分析；并观察能否通过干预CD40/CD40L协同刺激信号的方法，调控母体血清及母胎界面局部Th1、Th2型细胞因子水平,形成维持正常妊娠所需的Th2型免疫偏倚,诱导母胎免疫耐受。进一步揭示DC在流产中作用机制，对防治流产有极其重要的意义。

The occurrence of unknown recurrent spontaneous abortion(URSA) is related to disbalance of maternal-fetal immunoloregulation. Dendritic cell (DC) participates in regulating maternal-fetal tolerance, however, the mechanism is unclear. Our preliminary studies show that: in a graft versus host disease model, DC presents antigen to T cells in spleen and lymph nodes and induce T cells proliferation, the proliferated T cells migrate to target organs and then attack them causing injuries. On the basis of it, we want to use classical natural abortion mice models this time, using the method of injecting CD40 monoclonal antibody and CD40L monoclonal antibody, to observe that in the different status such as normal pregnancy, abortion or intervening the costimulating signal CD40/CD40L, the changes of DC's molecular expressions and DC's antigen presentation function: whether DC would make clusters with T cells and then cause T cells proliferation; whether proliferated T cells would migrate to maternal-fetal interface. The results should be contrasted with the preliminary studies and analysed. We also want to observe in this research that whether we can regulate the Th1 and Th2 type cytokines levels in maternal serum and on local maternal-fetal interface by means of intervening the costimulating signal CD40/CD40L and then to form the type Th2 immune bias, which is necessory in maintaining normal pregnancy, in order to induce maternal-fetal immunological tolerance. This research is extremely significant in revealing the mechanism of action of DC in abortion and providing a method to treat URSA .