CELL INTELLIGENCE · 肿瘤细胞治疗研究
肿瘤细胞治疗研究
英文原题：Immunosuppressive mechanisms and therapeutic targeting of regulatory T cells in ovarian cancer.
Immunosuppressive mechanisms and therapeutic targeting of regulatory T cells in ovarian cancer.
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卵巢癌仍然是最致命的妇科恶性肿瘤，这主要归因于其晚期诊断和免疫抑制性肿瘤微环境（TME）。卵巢癌免疫逃逸的一个关键介质是调节性T细胞（Tregs）的浸润和活化，其抑制抗肿瘤免疫并促进治疗耐药。针对Tregs的新兴治疗策略——如细胞因子调节、检查点阻断、代谢抑制剂和表观遗传调节剂——其恢复抗肿瘤免疫的潜力受到严格评估。本综述综合了关于卵巢TME如何塑造Treg生物学的最新进展，重点阐述了细胞因子信号传导、趋化因子驱动的募集、代谢重编程和免疫检查点相互作用等机制，以及肿瘤浸润Tregs的表型和功能异质性，包括组织驻留和滤泡亚群，及其响应肿瘤抗原的克隆扩增。通过阐明Tregs与卵巢TME之间的动态串扰，本综述为开发新型免疫疗法以克服Treg介导的免疫抑制并改善临床结局提供了框架。
Ovarian cancer remains the most lethal gynecologic malignancy, largely due to its late-stage diagnosis and immunosuppressive tumor microenvironment (TME). A key mediator of immune evasion in ovarian cancer is the infiltration and activation of regulatory T cells (Tregs), which suppress antitumor immunity and foster therapeutic resistance. Emerging therapeutic strategies to target Tregs-such as cytokine modulation, checkpoint blockade, metabolic inhibitors, and epigenetic regulators-are critically evaluated for their potential to restore antitumor immunity.
This review synthesizes recent advances in understanding how the ovarian TME shapes Treg biology, highlighting mechanisms such as cytokine signaling, chemokine-driven recruitment, metabolic reprogramming, and immune checkpoint interactions, as well as the phenotypic and functional heterogeneity of tumor-infiltrating Tregs, including tissue-resident and follicular subsets, and their clonal expansion in response to tumor antigens.
By elucidating the dynamic crosstalk between Tregs and the ovarian TME, this review provides a framework for developing novel immunotherapies to overcome Treg-mediated immunosuppression and improve clinical outcomes.
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