T cells. Within tumors, these alterations promote immune evasion through SASP-derived IL-6 and TGF-β, expand myeloid-derived suppressor cells, and favor angiogenic and immunosuppressive macrophage states. Cytotoxic lymphocyte and NK-cell dysfunction further weakens antitumor immunity and limits the responses to checkpoint inhibitors and chimeric Ag receptor T-cell therapy in older patients. In this review, we summarize the cellular and molecular mechanisms underlying immune cell aging and outline how immunosenescence programs reshape the tumor microenvironment and influence cancer immunotherapy outcomes.
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Oh et al. (2026) studied this question.
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