子宫内膜异位症的免疫机制研究进展

子宫内膜异位症(endometriosis,EMs)是以慢性盆腔痛、痛经、性交痛及不孕为主要症状的妇科常见病,目前该病的发病机制尚不清楚。研究表明腹腔微环境的异常免疫反应对异位内膜细胞的黏附、侵袭及血管生成至关重要。异位内膜的生长聚集大量多样性的免疫细胞,引发强烈的炎症反应,其中促炎因子、生长因子和血管生成增加。几乎所有类型的免疫细胞在EMs患者中都表现出了异常的免疫功能,如T细胞反应性和自然杀伤(NK)细胞毒性降低,B细胞的多克隆激活和抗体产生增加,腹腔巨噬细胞的数量和活化增加以及炎性介质的变化。进一步的探讨异位内膜细胞介导的免疫系统稳态失衡的机制,深层次了解异位内膜引发的免疫逃逸机制,可能成为新型非激素治疗的目标,从而制定出更全面的治疗EMs的方法。

Research Progress on Immune Mechanism of Endometriosis

Endometriosis is a common gynecological disease with chronic pelvic pain, dysmenorrhea, coital pain and infertility as the main symptoms, the pathogenesis of which is not yet clear. Studies have shown that abnormal immune responses in the peritoneal microenvironment are essential for attachment, invasion and angiogenesis of ectopic endometrial cells. The growth of ectopic endometrium accumulates a large number of diverse immune cells, triggering a strong inflammatory response in which pro-inflammatory cytokines, growth factors, and angiogenesis increase. Almost all types of immune cells exhibit abnormal immune functions in patients with endometriosis, such as T-cell reactivity and natural killer (NK) cell toxicity decreased, B cell polyclonal activation and antibody production increased, the number and activation of peritoneal macrophages increased and changes in inflammatory mediators. Further study on the mechanism of homeostatic imbalance of the immune system mediated by ectopic endometrium and understanding the mechanism of immune escape induced by ectopic endometrium may become the target of new non-hormone therapy，so as to develop a more comprehensive approach to treat EMs.