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A microsphere-vesicle hybrid system for tumor treatment through enhancement of innate and adaptive immune responses
Yida Chen1, Xinyi Cheng1, Can Zhu1
1Department of Orthopedics, The First Affiliated Hospital of Soochow University, Orthopedic Institute of Soochow University, Medical College of Soochow University, 899 Pinghai Road, Suzhou, Jiangsu, 215031, PR China.
Cancer immunotherapies, designed to modulate innate and/or adaptive immune responses alongside targeting immune checkpoint pathways, are hindered by the immunosuppressive properties of the tumor microenvironment (TME). In the present study, we developed a therapeutic system composed of TIM-3 antibody-loaded gelatin methacrylated (GelMA) microspheres conjugated with K7M2 osteosarcoma cell-derived vesicles containing EZH2 inhibitor EPZ6438 via an MMP2-responsive peptide sequence DPG. The hybrid system not only directly kills tumor cells and indirectly amplifies anticancer immunity, but also reprograms the TME by promoting tumor-associated macrophage polarization to the M1 phenotype, enhancing tumor-associated dendritic cell activation and blocking TIM-3-mediated immune suppression. Altogether, the engineered system releases both the drugs and antibodies to promote tumor apoptosis and reprograms the TME via modulation of innate and adaptive immunity, providing a promising and innovative therapeutic system for tumor treatment, and advancing the field of cancer immunotherapy.
Cancer immunotherapies, designed to modulate innate and/or adaptive immune responses alongside targeting immune checkpoint pathways, are hindered by the immunosuppressive properties of the tumor microenvironment (TME). In the present study, we developed a therapeutic system composed of TIM-3 antibody-loaded gelatin methacrylated (GelMA) microspheres conjugated with K7M2 osteosarcoma cell-derived vesicles containing EZH2 inhibitor EPZ6438 via an MMP2-responsive peptide sequence DPG. The hybrid system not only directly kills tumor cells and indirectly amplifies anticancer immunity, but also reprograms the TME by promoting tumor-associated macrophage polarization to the M1 phenotype, enhancing tumor-associated dendritic cell activation and blocking TIM-3-mediated immune suppression. Altogether, the engineered system releases both the drugs and antibodies to promote tumor apoptosis and reprograms the TME via modulation of innate and adaptive immunity, providing a promising and innovative therapeutic system for tumor treatment, and advancing the field of cancer immunotherapy.
