我们前期的研究已经证实腹腔巨噬细胞全面介入EMS发病过程，但研究发现EMS在位子宫内膜上皮细胞并不像正常子宫内膜上皮细胞一样引起巨噬细胞的显著极化；免疫抑制的巨噬细胞在EMS中的作用机制尚不清楚。本项目以EMS患者及模型小鼠为对象，首先明确EMS免疫抑制状态及DC-SIGN+巨噬细胞在EMS中的分布及CSF-1的表达情况；然后流式分选获得CD169+CSF-1R+DC-SIGN+巨噬细胞，将其与分选获得的NaïveT细胞共培养，观察T细胞中Treg细胞及CD8+T细胞的分化状况，并通过体外细胞系实验寻找CD169+CSF-1R+DC-SIGN+巨噬细胞形成的可能信号通路；通过动物模型中阻断巨噬细胞向免疫抑制CD169+CSF-1R+DC-SIGN+巨噬细胞分化的可能信号通路靶点，体内验证DC-SIGN+巨噬细胞在EMS免疫抑制过程中的作用，为阐明免疫抑制与EMS发病之间的关系提供实验依据。

Our researches have confirmed that the abdominal cavity macrophages have comprehensively intervene in the EMS process, but a new study has found that eutopic endometrial epithelial cells of endometriosis do not like a normal endometrial epithelial cells can induce macrophage polarize remarkably; In EMS, the mechanism of immune abnormal (mainly immunosuppressive) macrophages is not clear. Patients with EMS and model mice are the main study object, this project intends to confirm the immunosuppressive state of EMS, describes the distribution of CD169+MCSFR+DC-SGN+ immunosuppressive macrophages and the expression of CSF-1; Then, we obtain the CD169+MCSFR+DC-SGN+ immunosuppressive macrophages and naïve T cells by fluorescence-activated cell sorting(FACS) and co-culture with each other, describe the differentiation status of T cells, and through the in vitro cell line study, we can find a signal pathway for the induction of CD169+MCSFR+DC-SGN+ immunosuppressive macrophages. By blocking the targets of CD169+MCSFR+DC-SGN+ immunosuppressive macrophages differentiation signal pathway in in animal models, we can verify the role of DC-SGN+ immunosuppressive macrophages in EMS in vivo, and provide experimental basis of clarifying the relationship between immunosuppression and EMS.