免疫功能异常在子宫内膜异位症内膜容受性中研究进展

The Research Progress on Immune Dysfunction in Endometrial Receptivity of Endometriosis

近年子宫内膜异位症合并不孕的发病率升高,但其发病的分子机制尚不完全清楚。子宫内膜异位症合并不孕的患者常伴有局部或全身体液免疫、细胞免疫功能异常。主要表现为CD56+CD16-子宫自然杀伤细胞(uNK细胞)亚群显著减少,巨噬细胞活化异常,辅助性T细胞1(Th1)/Th2型细胞失衡,调节性T细胞(Treg)数量增加和功能缺陷,白血病抑制因子(LIF)表达减少,白细胞介素1(IL-1)、IL-6、γ干扰素(IFN-γ)和肿瘤坏死因子α(TNF-α)等细胞因子异常升高,导致免疫抑制和免疫不平衡状态,从而抑制细胞凋亡途径,促进异位子宫内膜细胞的黏附和增殖以及子宫内膜异位症病灶的血管生成,使子宫内膜容受性降低进而导致不孕。综述免疫功能异常在子宫内膜异位症内膜容受性中的研究进展,为子宫内膜异位症合并不孕的诊治提供新的思路。

In recent years,the incidence of endometriosis-induced infertility is increasing,the molecular mechanisms involved in the pathogenesis of endometriosis are not completely understood.These patients are often accompanied with local or whole body humoral immunity and cellular immune dysfunction,mainly showing significant reduction in CD56+CD16-uterine natural killer cell(uNK cell)subsets,abnormal activation of macrophage,imbalance of helper T cell 1(Th1)/Th2 cell,greater numbers of regulatory T cells(Treg)and dysfunction,reduced expression of leukemia inhibitory factor(LIF),and abnormally increased cytokines,such as interleukin-1(IL-1),IL-6,interferon-γ(IFN-γ)and tumor necrosis factorα(TNF-α).These are mainly manifested as immunosuppression and immune imbalance,which inhibit apoptotic pathways and promote adhesion and proliferation of endometriotic cells,as well as angiogenesis in endometriotic lesions.Therefore,these lead to the reduction of endometrial receptivity and cause infertility.This review summarizes the progress about immune dysfunction in endometrial receptivity of endometriosis,aiming to provide new ideas for the diagnosis and treatment of endometriosis with infertility.