Programmed death (PD)-1 is an inhibitory receptor expressed on activated T cells, B cells and myeloid cells. PD-1-deficient mice (Pdcd1 2/2 ) develop various spontaneous autoimmune diseases, including glomerulonephritis and dilated cardiomyopathy, indicating that this receptor plays a critical role in maintenance of peripheral tolerance [6] . PD-L1 (B7-H1) and PD-L2 (B7-DC), two immunoregulatory molecules belonging to the B7 superfamily, were identified as ligands for PD-1, engagement of PD-1 with its ligands mediates negative signaling events via recruitment of phosphatases, such as SHP-2, and dephosphorylation of some effector molecules involved in downstream T cell receptor (TCR) signaling [7, 8] .