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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.

OX40 (CD134) is a co-stimulatory receptor expressed on the surface of CD4+ and CD8+ T cells 24 to 48 hours after activation. Binding of OX40 to its ligand, OX40L (CD252), present on dendritic cells, potentiates T cell survival and increases cytokine production. OX40 has been shown to activate NF-κB-mediated memory cell generation through its interaction with adaptor proteins TRAF2 and TRAF5. OX40 has a critical role in the maintenance of an immune response beyond the first few days and onwards to a memory response.

Figure 1. Recombinant PD-1/OX40 Dual Effector Reporter Cell constitutively expressing OX40.

Figure 2. Recombinant PD-1/OX40 Dual Effector Reporter Cell constitutively expressing PD-1.

Figure 3. Dose Response of Blocking Antibodies in PD-1/OX40 Dual Effector Reporter Cells (C22) With PD-L1 aAPC Cells.