Abstract:

Premature ovarian insufficiency (POI) is a major disorder characterized by the decline of ovarian reserve function in reproductive-aged women. Its pathogenesis involves multiple factors, including immune dysregulation, genetic predisposition, infectious agents, and iatrogenic interventions. Aberrant cellular immunity is recognized as one of the critical etiological drivers of POI. As a key subset of lymphocytes in cellular immune responses, the helper T cells (Th cells) play a pivotal role in regulating ovarian endocrine function and folliculogenesis through the mechanisms of differentiation and immune regulation. Among Th cell subsets, Th17 cells and their signature cytokine, interleukin-17A (IL-17A), have emerged as the central players in the immunological pathogenesis of POI. Th17 cells secrete the pro-inflammatory cytokine IL-17A, which directly induces local ovarian inflammation and disrupts tissue architecture. Additionally, they also impair the follicular microenvironment, thereby compromising the granulosa cell function and leading to the reduction in ovarian reserve. Furthermore, Th17 cells disrupt immune homeostasis, thereby promoting the autoimmune injury that ultimately results in ovarian insufficiency. This target may become a potential novel immunotherapy strategy for POI.

Key words: Premature ovarian insufficiency, Ovarian reserve, Th17 cells, Interleukin-17, Granulosa cells