CELL INTELLIGENCE · 肿瘤细胞治疗研究

Immune cell senescence in ovarian cancer manifests as distinct phenotypic alterations in T cells, natural killer (NK) cells, macrophages, and dendritic cells (DCs), alongside dynamic crosstalk with the tumor microenvironment (TME). This senescence contributes substantially to the high mortality and therapeutic resistance characteristic of ovarian carcinoma. Senescent immune cells develop a senescence-associated secretory phenotype (SASP), secreting pro-tumorigenic cytokines and chemokines that drive regulatory T cell (Treg) expansion, extracellular matrix (ECM) remodeling, and the establishment of an immunosuppressive niche. Key drivers of immunocyte senescence include telomere erosion, epigenetic dysregulation, metabolic stress, DNA damage from chemotherapy, and chronic inflammatory signals. Emerging interventions, such as senolytic agents to selectively eliminate senescent immune cells, senomorphic compounds to attenuate SASP factors, and strategies to reprogram immune effectors, hold promise for restoring antitumor immunity and overcoming resistance to conventional therapies. A deeper understanding of the molecular mechanisms governing immunosenescence will be critical for the rational design of combination regimens and the development of next-generation immunotherapies in ovarian cancer.