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Mechanistic model of the action of monoclonal antibodies against immune molecules in GBM therapy. Classical immune checkpoints such as CTLA-4, PD-1, B7-H6, B7-H4, and TIM-3 bind to their ligands to inhibit T-cell activation and proliferation, thereby creating an immunosuppressive microenvironment. Blocking these immune checkpoint molecules by single or combination therapy with monoclonal antibodies may serve as a potential treatment for glioblastoma.
