This study reports the development of a heterojunction sonosensitizer (CD/TiSe₂) for in situ chemodynamic therapy (CDT) enhanced by sono-immunotherapy. TiSe₂ nanoplates, prepared through a one-step oil phase process, exhibit enhanced sonodynamic properties due to their narrow bandgap (1.62 eV), which facilitates electron-hole pair separation under low-intensity ultrasound (US) irradiation. In acidic tumor microenvironment (TME), TiSe₂ undergoes in situ redox reactions, forming TiO₂Se₂₋ₓ nanoplates containing Se (0), selenate, and Ti³⁺/Ti⁴⁺ redox couples. This redox couple facilitates in situ CDT through a Fenton-like reaction and consumes overexpressed glutathione (GSH) via Ti⁴⁺-mediated depletion. Additionally, Se ions promote dendritic cell (DC) maturation, activating adaptive immune responses. The construction of heterojunctions between carbon dots (CDs) and TiSe₂ further enhances ROS generation efficiency, amplifying the chemodynamic performance. The ROS produced by in situ CDT and sonodynamic therapy trigger immunogenic cell death (ICD) through a synergistic therapy, enhancing antitumor immunity with immune checkpoint blockade. This work provides a novel paradigm for in situ CDT-enhanced sono-immunotherapy using transition metal selenide-based sonosensitizers.This study reports the development of a heterojunction sonosensitizer (CD/TiSe₂) for in situ chemodynamic therapy (CDT) enhanced by sono-immunotherapy. TiSe₂ nanoplates, prepared through a one-step oil phase process, exhibit enhanced sonodynamic properties due to their narrow bandgap (1.62 eV), which facilitates electron-hole pair separation under low-intensity ultrasound (US) irradiation. In acidic tumor microenvironment (TME), TiSe₂ undergoes in situ redox reactions, forming TiO₂Se₂₋ₓ nanoplates containing Se (0), selenate, and Ti³⁺/Ti⁴⁺ redox couples. This redox couple facilitates in situ CDT through a Fenton-like reaction and consumes overexpressed glutathione (GSH) via Ti⁴⁺-mediated depletion. Additionally, Se ions promote dendritic cell (DC) maturation, activating adaptive immune responses. The construction of heterojunctions between carbon dots (CDs) and TiSe₂ further enhances ROS generation efficiency, amplifying the chemodynamic performance. The ROS produced by in situ CDT and sonodynamic therapy trigger immunogenic cell death (ICD) through a synergistic therapy, enhancing antitumor immunity with immune checkpoint blockade. This work provides a novel paradigm for in situ CDT-enhanced sono-immunotherapy using transition metal selenide-based sonosensitizers.