Endometriosis is a common estrogen-dependent condition affecting 8–10% of women of reproductive age, causing pain, morbidity, and infertility. Despite extensive research, its exact cause remains unclear, and the mechanisms behind its associated infertility are not fully understood. Natural killer (NK) cells, crucial for successful pregnancy, have been investigated for their role in endometriosis pathogenesis. Recent evidence suggests NK cells regulate endometrial stromal cells (ESCs), promoting immune tolerance, influencing endometrial receptivity, oocyte development, and embryo implantation, thereby contributing to infertility and miscarriage in endometriosis patients. This review summarizes current literature on the role of NK cells in endometriosis, particularly in infertility and pregnancy loss, under estrogen influence. Estrogen influences NK cell function through direct and indirect mechanisms, affecting their recruitment, proliferation, differentiation, and activity. In endometriosis, estrogen levels are elevated, leading to altered NK cell function, including reduced cytotoxicity and impaired immune surveillance. These changes may contribute to the persistence of endometriotic lesions and adverse reproductive outcomes. Estrogen also regulates the expression of cytokines and chemokines that influence angiogenesis and vascularization of ectopic lesions. In endometriosis, NK cells exhibit altered phenotypes and functions, including reduced cytotoxicity and increased expression of inhibitory receptors. These changes may impair immune surveillance and promote immune evasion by ectopic endometrial cells. Estrogen signaling also affects the expression of cytokines such as IL-15 and Galectin-3, which regulate ESC adhesion, migration, and invasion. Estrogen-NK cell interactions play a critical role in immune regulation in endometriosis. Estrogen can induce the differentiation of COX-2+ NK cells, which produce PGE2 and promote Treg cell differentiation, contributing to immunotolerance and endometriotic lesion persistence. Estrogen also influences the expression of cytokines such as IL-10 and TGF-β, which suppress immune responses and promote immunotolerance. In endometriosis-related infertility and miscarriage, estrogen-NK cell interactions may impair oocyte maturation, embryo development, and implantation. NK cells in peritoneal fluid have been shown to exert embryotoxic effects, inhibiting fertilization and embryo development. Estrogen may regulate NK cell-mediated embryotoxicity by modulating cytokine secretion. Estrogen-NK cell interactions also influence endometrial receptivity and implantation. In endometriosis, impaired NK cell function may lead to reduced endometrial receptivity and implantation failure. CD200S expression on NK cells is increased in endometriosis, potentially contributing to immune rejection of the embryo. Overall, the estrogen-NK cell axis plays a significant role in the pathogenesis of endometriosis, infertility, and miscarriage. Understanding the mechanisms underlying these interactions isEndometriosis is a common estrogen-dependent condition affecting 8–10% of women of reproductive age, causing pain, morbidity, and infertility. Despite extensive research, its exact cause remains unclear, and the mechanisms behind its associated infertility are not fully understood. Natural killer (NK) cells, crucial for successful pregnancy, have been investigated for their role in endometriosis pathogenesis. Recent evidence suggests NK cells regulate endometrial stromal cells (ESCs), promoting immune tolerance, influencing endometrial receptivity, oocyte development, and embryo implantation, thereby contributing to infertility and miscarriage in endometriosis patients. This review summarizes current literature on the role of NK cells in endometriosis, particularly in infertility and pregnancy loss, under estrogen influence. Estrogen influences NK cell function through direct and indirect mechanisms, affecting their recruitment, proliferation, differentiation, and activity. In endometriosis, estrogen levels are elevated, leading to altered NK cell function, including reduced cytotoxicity and impaired immune surveillance. These changes may contribute to the persistence of endometriotic lesions and adverse reproductive outcomes. Estrogen also regulates the expression of cytokines and chemokines that influence angiogenesis and vascularization of ectopic lesions. In endometriosis, NK cells exhibit altered phenotypes and functions, including reduced cytotoxicity and increased expression of inhibitory receptors. These changes may impair immune surveillance and promote immune evasion by ectopic endometrial cells. Estrogen signaling also affects the expression of cytokines such as IL-15 and Galectin-3, which regulate ESC adhesion, migration, and invasion. Estrogen-NK cell interactions play a critical role in immune regulation in endometriosis. Estrogen can induce the differentiation of COX-2+ NK cells, which produce PGE2 and promote Treg cell differentiation, contributing to immunotolerance and endometriotic lesion persistence. Estrogen also influences the expression of cytokines such as IL-10 and TGF-β, which suppress immune responses and promote immunotolerance. In endometriosis-related infertility and miscarriage, estrogen-NK cell interactions may impair oocyte maturation, embryo development, and implantation. NK cells in peritoneal fluid have been shown to exert embryotoxic effects, inhibiting fertilization and embryo development. Estrogen may regulate NK cell-mediated embryotoxicity by modulating cytokine secretion. Estrogen-NK cell interactions also influence endometrial receptivity and implantation. In endometriosis, impaired NK cell function may lead to reduced endometrial receptivity and implantation failure. CD200S expression on NK cells is increased in endometriosis, potentially contributing to immune rejection of the embryo. Overall, the estrogen-NK cell axis plays a significant role in the pathogenesis of endometriosis, infertility, and miscarriage. Understanding the mechanisms underlying these interactions is