国际生殖健康/计划生育杂志 ›› 2025, Vol. 44 ›› Issue (6): 501-505.doi: 10.12280/gjszjk.20250487

• 综述 • 上一篇    下一篇

Th17细胞及IL-17A在早发性卵巢功能不全中的作用

张茜蒻, 王荣荣, 苏婧, 薛凤霞()   

  1. 300052 天津医科大学总医院妇产科,天津市女性生殖健康与优生重点实验室
  • 收稿日期:2025-09-19 出版日期:2025-11-15 发布日期:2025-11-18
  • 通讯作者: 薛凤霞,E-mail:xuefengxia@tmu.edu.cn

The Role of Th17 Cells and IL-17A in the Pathogenesis of Premature Ovarian Insufficiency

ZHANG Xi-ruo, WANG Rong-rong, SU Jing, XUE Feng-xia()   

  1. Department of Obstetrics and Gynecology, Tianjin Key Laboratory of Female Reproductive Health and Eugenics, Tianjin Medical University General Hospital, Tianjin 300052, China
  • Received:2025-09-19 Published:2025-11-15 Online:2025-11-18
  • Contact: XUE Feng-xia, E-mail: xuefengxia@tmu.edu.cn

摘要:

早发性卵巢功能不全(premature ovarian insufficiency,POI)是导致育龄期女性卵巢储备功能减退的疾病之一,其发病机制涉及免疫、遗传、感染、医源性等多种因素,自身免疫异常是导致POI的重要原因之一。辅助性T细胞(T helper cell,Th细胞)作为细胞免疫应答的重要淋巴细胞亚群,其分化调节、免疫功能与卵巢内分泌功能和卵泡生长发育密切相关,其中Th17细胞及其分泌的细胞因子白细胞介素-17A(interleukin-17A,IL-17A)在自身免疫性POI的发病中具有重要作用。Th17细胞可通过分泌促炎细胞因子IL-17A直接介导卵巢局部炎症损伤,破坏卵巢组织结构或卵泡发育微环境,影响颗粒细胞功能,导致卵巢储备功能减退;也可通过打破免疫平衡,诱导自身免疫损伤,最终导致卵巢功能衰退。该靶点或可用于POI的新型免疫治疗策略。

关键词: 原发性卵巢功能不全, 卵巢储备功能, Th17细胞, 白细胞介素17, 粒层细胞

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