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The impact of endometriosis and adenomyosis on reproduction and pregnancy is significant, with both conditions linked to increased rates of infertility, poor ovarian function in women with endometriosis, and elevated pregnancy complications in those with adenomyosis. However, the underlying mechanisms remain largely unclear. Both conditions share a similar pathophysiological process characterized by the growth of ectopic endometrium, which may originate from the eutopic endometrium. Notably, surgical removal of ectopic lesions does not appear to significantly improve reproductive and pregnancy outcomes, further underscoring the importance of eutopic endometrium in these adverse effects. Emerging evidence indicates substantial differences in endometrial NK cells, macrophages, and T cells, leading to inflammatory responses in women with endometriosis and adenomyosis. These alterations may contribute not only to disease progression but also to defective endometrial receptivity, insufficient angiogenesis remodeling, impaired maternal-fetal immune tolerance, and poor placentation, thereby influencing embryo implantation and pregnancy maintenance. This provides an immunological perspective to explain the higher rates of infertility and pregnancy complications observed in affected women. Therefore, we systematically review the alterations in endometrial immune cells in women with endometriosis and adenomyosis compared to healthy controls, exploring the potential impacts of these changes on reproduction and pregnancy. This review aims to lay the groundwork for future studies on the immunopathogenesis associated with endometriosis and adenomyosis-related reproductive failure and pregnancy complications, shedding lights on the development of immunotherapeutic strategies to mitigate these adverse impacts in affected women.
Shi et al. (Tue,) studied this question.