子宫内膜异位症（Endometrisosis，EM）发病率和复发率高，严重影响患者身心健康，但其发病机制不明确。腹腔巨噬细胞在EM进程中发挥重要作用，然而，EM中腹腔巨噬细胞的吞噬能力减弱、且功能分化状态不明确。我们在前期基础中发现大腹腔巨噬细胞具有更强的抑制EM进展的潜力，且异位内膜组织的CD47表达升高。因此，我们从腹腔巨噬细胞新亚型角度开辟新的研究切入点，利用视黄酸诱导巨噬细胞亚型转化，进而增强总腹腔巨噬细胞的吞噬能力和M1功能极化潜力。此外，我们将整合免疫治疗领域的前沿热点，探讨基于巨噬细胞免疫检查点阻断治疗EM的可能性，阐明CD47-SIRPα通路在EM进程中的变化规律，进而明确CD47在逃避巨噬细胞吞噬中的作用机理，利用抗体阻断该通路研究其对EM进程的影响。上述两种治疗方案均基于调控腹腔巨噬细胞，我们将探究联合治疗的优势。本项目既深化EM发病机制研究，又探索EM新治疗策略。

Endometriosis (EM) incidence and recurrence rates are high, thereby seriously affecting patients’ physical and mental health. However, EM’s pathogenesis is not clear. Peritoneal macrophages play an important role in the EM process, but their phagocytic ability is weakened, and the state of functional differentiation is unclear. In our previous study, we found that large peritoneal macrophage had a great potential to inhibit EM progression, and CD47 expression in ectopic endometrial tissue is elevated. Therefore, we have opened a new research entry point from the perspective of new subtypes of peritoneal macrophages. Macrophage subtype transformation through retinoic acid is performed, thereby enhancing the phagocytic capacity and M1 functional polarization potential of total peritoneal macrophages. In addition, we integrate the frontier hotspots in immunotherapy, explore the possibility of blocking EM based on macrophage immunological checkpoints, and use EM animal models and clinical samples to clarify the changes in the CD47–SIRPα pathway in the EM process. We also study the underlying mechanism of CD47’s evasion of macrophage phagocytosis by CD47-gene-modified cells. Then, we will use antibodies to block this pathway to study its effect on EM progression. Both treatments are based on the regulation of peritoneal macrophages, and we explore the advantages of combination therapy. This project not only deepens the research on the pathogenesis of EM, but also explores a new treatment strategy of EM.