Programmed cell death (PCD) is a conserved mechanism of cell suicide that plays a critical role in various biological processes, including immunity and cancer development. PCD includes apoptosis, autophagy-dependent cell death, pyroptosis, ferroptosis, and necroptosis, and these processes have significant implications for tumor immunity. PCD can modulate the function of immune cells, leading to immunological outcomes such as tumor-specific T cell priming, immunosuppression, and immune evasion. Targeting PCD alone or in combination with conventional immunotherapy may enhance the efficacy of anticancer treatments. This review discusses the characteristics and mechanisms of PCD pathways, their interactions with tumor immunity, and the therapeutic potential of PCD-based approaches in cancer treatment. Apoptosis, a well-studied form of PCD, is regulated by extrinsic and intrinsic pathways. The extrinsic pathway involves death receptors and caspase-8 activation, while the intrinsic pathway is mediated by mitochondrial dysfunction and cytochrome c release. Pyroptosis, a form of inflammatory cell death, is triggered by inflammasome activation and involves the release of proinflammatory factors. Ferroptosis is characterized by iron accumulation and lipid peroxidation, while necroptosis is a caspase-independent form of cell death involving RIPK1, RIPK3, and MLKL. Autophagy-dependent cell death is a complex process that can either promote or inhibit cell death, depending on the context. The crosstalk between PCD and the tumor microenvironment (TME) is crucial for tumor immunity. Apoptosis can stimulate antitumor immune responses by activating immune cells and promoting the release of proinflammatory mediators. However, it can also contribute to immunosuppression by facilitating the clearance of apoptotic cells and promoting the infiltration of immunosuppressive cells. Autophagy-dependent cell death can influence the tumor immune microenvironment by modulating macrophage polarization and the response to immunotherapy. Pyroptosis can enhance antitumor immunity by activating dendritic cells and promoting T cell expansion, while necroptosis can lead to immunosuppression by releasing DAMPs and activating immunosuppressive cells. Understanding the role of PCD in tumor immunity is essential for developing effective cancer therapies. Targeting PCD pathways may provide new strategies to enhance the efficacy of immunotherapy and improve patient outcomes. Further research is needed to elucidate the complex interactions between PCD and the immune system and to translate these findings into clinical applications.Programmed cell death (PCD) is a conserved mechanism of cell suicide that plays a critical role in various biological processes, including immunity and cancer development. PCD includes apoptosis, autophagy-dependent cell death, pyroptosis, ferroptosis, and necroptosis, and these processes have significant implications for tumor immunity. PCD can modulate the function of immune cells, leading to immunological outcomes such as tumor-specific T cell priming, immunosuppression, and immune evasion. Targeting PCD alone or in combination with conventional immunotherapy may enhance the efficacy of anticancer treatments. This review discusses the characteristics and mechanisms of PCD pathways, their interactions with tumor immunity, and the therapeutic potential of PCD-based approaches in cancer treatment. Apoptosis, a well-studied form of PCD, is regulated by extrinsic and intrinsic pathways. The extrinsic pathway involves death receptors and caspase-8 activation, while the intrinsic pathway is mediated by mitochondrial dysfunction and cytochrome c release. Pyroptosis, a form of inflammatory cell death, is triggered by inflammasome activation and involves the release of proinflammatory factors. Ferroptosis is characterized by iron accumulation and lipid peroxidation, while necroptosis is a caspase-independent form of cell death involving RIPK1, RIPK3, and MLKL. Autophagy-dependent cell death is a complex process that can either promote or inhibit cell death, depending on the context. The crosstalk between PCD and the tumor microenvironment (TME) is crucial for tumor immunity. Apoptosis can stimulate antitumor immune responses by activating immune cells and promoting the release of proinflammatory mediators. However, it can also contribute to immunosuppression by facilitating the clearance of apoptotic cells and promoting the infiltration of immunosuppressive cells. Autophagy-dependent cell death can influence the tumor immune microenvironment by modulating macrophage polarization and the response to immunotherapy. Pyroptosis can enhance antitumor immunity by activating dendritic cells and promoting T cell expansion, while necroptosis can lead to immunosuppression by releasing DAMPs and activating immunosuppressive cells. Understanding the role of PCD in tumor immunity is essential for developing effective cancer therapies. Targeting PCD pathways may provide new strategies to enhance the efficacy of immunotherapy and improve patient outcomes. Further research is needed to elucidate the complex interactions between PCD and the immune system and to translate these findings into clinical applications.