Fig. 2

The interaction between the TCR and the tumor-specific antigen shown in the context of MHC II results in T cell activation. Following the activation of a number of downstream targets that PD-1 releases in response to interaction with either of its ligands, programmed cell death-ligand 1 (PD-L1) or 2 (PD-L2), deactivation of T cells takes place, which ultimately leads to the suppression of cytotoxic T lymphocytes (CTL). While controlling CTL activity may work as a brake to lower the likelihood of autoimmunity against host antigens, inhibiting CTL activation will be employed by forming tumor cells to evade the host's immune surveillance, which will lead to the growth of the tumor. The interaction of ICIs mAbs to PD-1, PD-L1, PD-L2, and CTLA4 restores T cell activation and slows the growth of tumors