Cellular senescence offers distinct immunological vulnerabilities in cancer.

Chronic damage following oncogene induction or cancer therapy can produce cellular senescence. Senescent cells not only exit the cell cycle but communicate damage signals to their environment that can trigger immune responses. Recent work has revealed that senescent tumor cells are highly immunogenic, leading to new ways to activate antitumor immunosurveillance and potentiate T cell-directed immunotherapies. However, other studies have determined that heterogeneous senescent stromal cell populations contribute to immunosuppression and tumor progression, sparking the development of senotherapeutics to target senescent cells that evade immune detection. We review current findings that provide deeper insights into the mechanisms contributing to the dichotomous role of senescence in immune modulation and how that can be leveraged for cancer immunotherapy.