Reprogramming tumor-associated macrophages to an antitumor M1 phenotype by photodynamic therapyi s ap romising strategy to overcome the immunosuppression of tumor microenvironment for boosted immunotherapy. However,itremains unclear howthe reactive oxygen species (ROS) generated from type Ia nd II mechanisms,r elate to the macrophage polarization efficacy.H erein, we design and synthesize three donor-acceptor structured photosensitizers with varied ROS-generating efficiencies.S urprisingly,w e discovered that the extracellular ROS generated from type I mechanism are mainly responsible for reprogramming the macrophages from ap ro-tumor type (M2) to an anti-tumor state (M1). In vivo experiments prove that the photosensitizer can trigger photodynamic immunotherapyf or effective suppression of the tumor growth, while the therapeutic outcome is abolished with depleted macrophages.O verall, our strategy highlights the designing guideline of macrophage-activatable photosensitizers.