Photodynamic therapy (PDT) uses reactive oxygen species (ROS) generated by photosensitizers to destroy cancer cells. It induces local inflammation and activates the adaptive immune system, leading to tumor destruction and immune memory. This review summarizes recent findings on how PDT induces adaptive immunity through ROS. PDT involves administering a photosensitizer, which is activated by light to produce ROS, causing direct and indirect cancer cell death. ROS trigger the release of damage-associated molecular patterns (DAMPs), activating dendritic cells and T cells, which lead to immune responses against tumors. PDT also enhances the immune system by promoting the maturation of dendritic cells and cross-presentation of tumor antigens. However, the tumor microenvironment (TME) can suppress PDT's immune effects through immunosuppressive factors, hypoxia, and suppressor cells like myeloid-derived suppressor cells (MDSCs) and regulatory T cells. Recent studies show that PDT can be enhanced by combining it with other therapies, such as checkpoint inhibitors, chemotherapy, or photothermal therapy, to improve immune responses and cancer treatment outcomes. Despite progress, challenges remain, including the need for more effective photosensitizers and optimized treatment regimens. Future research should focus on improving PDT's ability to activate adaptive immunity and overcome TME resistance. Overall, PDT holds promise as a cancer therapy that can activate immune responses and prevent tumor recurrence.Photodynamic therapy (PDT) uses reactive oxygen species (ROS) generated by photosensitizers to destroy cancer cells. It induces local inflammation and activates the adaptive immune system, leading to tumor destruction and immune memory. This review summarizes recent findings on how PDT induces adaptive immunity through ROS. PDT involves administering a photosensitizer, which is activated by light to produce ROS, causing direct and indirect cancer cell death. ROS trigger the release of damage-associated molecular patterns (DAMPs), activating dendritic cells and T cells, which lead to immune responses against tumors. PDT also enhances the immune system by promoting the maturation of dendritic cells and cross-presentation of tumor antigens. However, the tumor microenvironment (TME) can suppress PDT's immune effects through immunosuppressive factors, hypoxia, and suppressor cells like myeloid-derived suppressor cells (MDSCs) and regulatory T cells. Recent studies show that PDT can be enhanced by combining it with other therapies, such as checkpoint inhibitors, chemotherapy, or photothermal therapy, to improve immune responses and cancer treatment outcomes. Despite progress, challenges remain, including the need for more effective photosensitizers and optimized treatment regimens. Future research should focus on improving PDT's ability to activate adaptive immunity and overcome TME resistance. Overall, PDT holds promise as a cancer therapy that can activate immune responses and prevent tumor recurrence.