越来越多的研究认为,免疫调节在子宫内膜异位症(EMs)的发生、发展过程中起重要作用,腹腔免疫微环境的变化是EMs发生的前提和腹腔症状的病理基础。巨噬细胞通过不同功能的分化和时序变化,通过腹腔免疫微环境影响EMs的血管生成和异位内膜成功植入的分子机制。腹腔微环境发生变化体现在特定的炎症反应过程,其中巨噬细胞功能的改变作为基础性因素,介入异位病灶和腹腔微环境之间。巨噬细胞的功能分化体现在其通过吞噬或促进凋亡以清除异位病灶的同时,对血管生成和子宫内膜植入产生促进作用。 More and more studies suggest that immune regulation plays an important role in the occurrence and development of endometriosis (EMs). The change of peritoneal immune microenvironment is the precondition of EMs and the pathological basis of peritoneal symptoms. Macrophages influence the angiogenesis of EMs and the molecular mechanism of successful implantation of ectopic endometrium through the peritoneal immune microenvironment through differentiation and timing changes of different functions. Changes in the peritoneal microenvironment reflected in the specific inflammatory response process, in which changes in macrophage function as a basic factor, interventional ectopic lesions and the peritoneal microenvironment between. The functional differentiation of macrophages manifests itself in promoting angiogenesis and endometrial implantation while phagocytosis or the promotion of apoptosis to clear ectopic lesions.