A cell surface receptor called Programmed Death-1 (PD-1) serves as a T cell checkpoint and is crucial in controlling T cell exhaustion. PDL-1 or PDL-2 engagement with PD-1 causes it to become active. When the PD-1 receptor binds to its ligands, PD-L1 and PD-L2, which are expressed on cancer cells and antigen-presenting cells, it sends inhibitory checkpoint signals to activated T cells. This suppresses T-cell effector function and allows tumor immune evasion. An appealing approach for tumor immunotherapy is to block the programmed cell death-1 (PD-1)/programmed cell death-ligand 1 (PD-L1) pathway.
Activated T cells, B cells, monocytes, dendritic cells, regulatory T cells, and natural killer T cells all express PD-1. It belongs to a group of immunoglobulin domain (Ig) co-receptors that affect how the T cell receptor responds when activated by an antigen-presenting cell (APC) or an infected target cell. In contrast to PD-L2, which is only and inducibly expressed on professional APCs, PD-L1 is widely expressed and constitutively on both hematopoietic and nonhematopoietic cells, including naive T and B cells, vascular endothelial cells, and pancreatic islet cells.
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