The binding of Programmed Cell Death Protein 1 (PD-1), a receptor expressed on activated T cells, to its ligands, PD-L1 and PD-L2, negatively regulates immune responses. The PD-1 ligands are found on most cancers, and PD-1:PD-L1/2 interaction inhibits T cell activity and allows cancer cells to escape immune surveillance. The PD-1:PD-L1/2 pathway is also involved in regulating autoimmune responses, making these proteins promising therapeutic targets for a number of cancers, as well as multiple sclerosis, arthritis, lupus, and type I diabetes.

B7-1, also known as CD80, is a membrane receptor found in activated antigen presenting cells (APC).

B7-2 (CD86) signaling through CTLA4 (CD152) has been shown to inhibit T- cell activation. This co-inhibitory pathway can be overactive in many tumors, enabling cancers to escape the host’s immune system. CTLA4-blocking antibodies, including Ipilimumab (Yervoy) and Tremelimumab, have shown clinical efficacy in treating cancer.

PD-1、CD80、CD86

RPMI-1640+10%FBS+1ug/ml puromycin+800ug/ml hygromycin

Figure 1. Dose Response of Blocking Antibodies in PD-1/CTLA4 Dual Effector Reporter Cells (C16) With PD-L1/CD80&CD86 aAPC Cells.