A Comprehensive Review of US FDA-Approved Immune Checkpoint Inhibitors in Urothelial Carcinoma

Figure 1

Illustration of anticheckpoint immunotherapy. The immune system is maintained and functions in homeostasis. Once CD28 binds to its ligand, B7, on the surface of antigen-presenting cells (APCs), T cell proliferation is activated to enhance immunity. On the other hand, cytotoxic T lymphocyte antigen-4 (CTLA-4) and programmed death-1 (PD-1) on APCs or tumor cells transmit inhibitory signals, while binding to their ligands, B7 and PD-L1, respectively. In general, the immune cells could recognize tumor cells and then destroy them. However, the tumor cells can escape from the host antitumor activities by suppressing the activation of immune cells. The anticheckpoint antibodies are developed to block the inhibitory pathways and then restore T cell immunity against tumors.