Interconnection between polycystic ovary syndrome, immune disorders, and reproductive outcomes
Abstract
Abstract: Polycystic ovary syndrome (PCOS) is a multifactorial disorder traditionally recognized for its endocrine and metabolic disturbances. However, accumulating evidence indicates that chronic low-grade inflammation and immune dysregulation play a central role in its pathophysiology. This narrative review explores the immunological mechanisms underlying PCOS and their repercussions for reproductive outcomes. Women with PCOS exhibit increased circulating levels of inflammatory cytokines - including interleukin (IL)-6, IL-1β, IL-18, and tumor necrosis factor-alpha (TNF-α) - alongside macrophage and lymphocyte infiltration within ovarian and endometrial tissues. These alterations promote oxidative stress, granulosa cell apoptosis, impaired steroidogenesis, and diminished endometrial receptivity. The adaptive immune response is similarly altered, characterized by imbalances between Th1/Th2 and Th17/regulatory T lymphocyte subsets and the presence of autoantibodies, including antinuclear, antithyroid, and antiphospholipid antibodies. These immune abnormalities have been associated with implantation failure and recurrent pregnancy loss. Furthermore, autoimmune diseases, including Hashimoto's thyroiditis and type 1 diabetes mellitus, occur more frequently among women with PCOS, reinforcing the concept of an underlying systemic immunometabolic imbalance. Unlike prior reviews, this work offers a novel integrative framework that connects systemic inflammation with localized immune…
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