Evolving Concepts: Immunity in Oncology from Targets to Treatments

Figure 2

Immune therapy in cancer: blocking CTLA4-B7 interactions to enhance T-cell activation could help overcome tumor antigen tolerance and consequently potentiate enhanced antitumoral responses. Blocking PD-1, PD-L1 allows for more B7 family members on immune cells such as CD80/CD86 to be available and bind CD28 (Figure 1) allowing for more activated effector T-cells capable to recognize and eliminate cells bearing cancer antigens. TCR: T-cell receptor; MHC: major histocompatibility antigen; IL-2: interleukin-2; CTLA4: cytotoxic T lymphocytes antigen-4; PD-1: programmed death-1 also known as CD279; PD-L1: programmed death-ligand 1 known as B7-H1 or CD274; PD-L2: programmed death-ligand 2, known as CD273 or B7-DC B-7 dendritic cell; IFN-γ: interferon gamma; IL-2: interleukin-2; APC: antigen presenting cells; TRY: tryptophan; AP-1: activator protein-1; NFAT: nuclear factor of activated T-cells; NFKB: nuclear factor kappa B; MAPK: mitogen activated protein kinase; IKK: I kappa B kinase; PI3K: phosphatidylinositol-4,5-biphosphate 3-kinase; CDK: cyclin dependant kinase; JAK3: Janus kinase 3; mTOR: mammalian target of rapamycin; anti-CTLA4: antibody blocking CTLA4; anti-PD-1: antibody blocking PD-1; anti-PD-L1: antibody blocking PD-L1.