PD-1 is an immune checkpoint and guards against autoimmunity through two mechanisms. PD-1 inhibitors, a new class of drugs that block PD-1, activate the immune system to programmed cell death protein 1 antibody tumors and are used to treat certain types of cancer.
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The PD-1 protein in humans is encoded by the PDCD1 gene. In a screen for genes involved in apoptosis, Yasumasa Ishida, Tasuku Honjo and colleagues at Kyoto University in 1992 discovered and named PD-1. PD-1 is a type I membrane protein of 268 amino acids. CTLA-4 family of T cell regulators. PD-1 has two ligands, PD-L1 and PD-L2, which are members of the B7 family. Several lines of evidence suggest that PD-1 and its ligands negatively regulate immune responses.
T cells are more susceptible to inhibition by PD-L1, although this could be dependent on the strength of TCR signaling. Expression of PD-L1 on tumor cells inhibits anti-tumor activity through engagement of PD-1 on effector T cells. Expression of PD-L1 on tumors is correlated with reduced survival in esophageal, pancreatic and other types of cancers, highlighting this pathway as a target for immunotherapy. In mice, expression of this gene is induced in the thymus when anti-CD3 antibodies are injected and large numbers of thymocytes undergo apoptosis. PD-L1, the ligand for PD1, is highly expressed in several cancers and hence the role of PD1 in cancer immune evasion is well established. Combination therapy using both anti-PD1 along with anti-CTLA4 therapeutics have emerged as important tumor treatments within the field of checkpoint inhibition.