Abstract: 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 factor α (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.

Key words: Endometriosis, Immunity, cellular, Cytokines, Infertility, female;, Endometrial receptivity