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Figure 2. Immunotherapeutic strategies for treatment of brain cancers. A: checkpoint blockade with monoclonal antibodies against PD-1 and CTLA-4 can block the interaction of these receptors with their ligands expressed on tumor cells leading to sustained T-cell activation and anti-tumor responses; B: vaccination therapy depends on dendritic cell antigen presentation of peptides or antigens derived from tumor lysates. In peptide vaccine therapy, peptides can be antigens encoded by mutant genes and thus be expressed only on tumor cells. These neoantigens are called TSA. Other peptides can be antigens derived from the modulated expression of normal peptides and are termed TAA. In cell-based vaccination, dendritic cells are expanded and activated ex vivo with patient-tumor lysates prior to administration. Both vaccine modalities aim to stimulate anti-tumor humoral and cellular immune responses; C: in CAR T-cell therapy, autologous T-cells are isolated and transfected with CAR construct, and transferred back into patients. These T-cells can recognize tumor-associated antigens obviating the need for MHC-dependent antigen presentation; D: oncolytic virus therapy allows the preferential replication of the virus in tumor cells causing tumor cell lysis and release of antigens that can induce an immune response. This figure contains images from Servier Medical Art. CAR: chimeric antigen receptor; CD: cluster of differentiation; CTLA-4: cytotoxic T-lymphocyte-associated protein-4; EGFRvIII: epidermal growth factor receptor variant III; HER2: human epidermal growth factor receptor 2; IL-13Rα2: interleukin-13 receptor alpha 2; MHC: major histocompatibility complex; PD-1: programmed cell death-1; PD-L1: programmed death-ligand 1; TAA: tumor-associated antigens; TCR: T-cell receptor; TSA: tumor-specific antigen