子宫内膜异位症（EMs）的病因至今未被阐明。异位定植的内膜组织得已存活，可能是EMs患者体内的免疫系统处于异常。本研究以前期工作为基础，通过分析异位细胞外泌体蛋白质谱，发现在外泌体中异常高表达的蛋白AOC3，已有文献支持AOC3可招募CD4+T细胞外渗至病灶。同时我们发现EMs患者的CD4+T细胞外泌体可诱导异位内膜表达PD-L1。因此，我们假设：异位内膜组织分泌外泌体AOC3募集CD4+T细胞至异位组织，而CD4+T细胞可分泌特异性外泌体miRNA诱导异位内膜表达PD-L1造成免疫逃逸。我们将过载AOC3氨基酸序列至外泌体，检测其对CD4+T细胞的趋向性。MiR测序寻找特异性诱导PD-L1表达的CD4+T细胞外泌体miRNA。通过IP及RPD技术确定介导免疫逃逸的分子通路，并在体内和体外实验中对各项指标进行分析。另外，将通过大样本量确定阴道分泌物中外泌体AOC3可作为EMs诊断标志物。

The pathogenesis of endometriosis has not yet been elucidated. The survival of ectopic endometrial tissue probably related to the abnormal immune system in EMs patients. Based on previous work, by analyzing the exosomal protein profiling from ectopic cells, this study found that AOC3 was aberrantly high expressed in the exosoms. By further exploring previous reports, it was found that AOC3 could recruit CD4+T cells to infiltrate into surrounding lesions Moreover, we found that CD4+T cells isolated from EMs patients and their secreted exosomes could induce the expression of PD-L1 in ectopic endometrial cells. Therefore, we hypothesized that exosomal AOC3 secreted by ectopic endometrium collected CD4+T cells to infiltrate around ectopic tissues, and CD4+T cells could secrete specific exosome miRNA to induce the expression of PD-L1 in ectopic endometrium tissues caused immune escape. We will overload AOC3 amino acid sequence into exosome to detect the tendency to CD4+T cells. MiR sequencing was used to search for specific exo-miR from CD4+T cell induced PD-L1 expression. The molecular pathway mediating immune escape were determined by IP and RNA PULL DOWN techniques, and the indicators were verified and analyzed by various experiments. In addition, we will confirm that exosomal AOC3 in vaginal secretion can be used as a non-invasive diagnostic marker for EMs using large sample size verification.