Programmed death-ligand 1 (PD-L1), or B7-H1, is a transmembrane, co-stimulatory ligand of programmed cell death protein 1 (PD-1) that, along with B7-1 and B7-2, belongs to the B7 family and immunoglobulin superfamily. Though more notably expressed on activated T-cells, B-cells, myeloid cells, and a subset of thymocytes, PD-L1 is also expressed constitutively by nonlymphoid, parenchymal organs, including the heart, placenta, skeletal muscle, and lung; with the marked exception of the small intestine. As a member of the B7 family, PD-L1 plays a principal role in immunity: suppressing immune response against autoantigens and tumors, maintaining T-cell homeostasis, maintaining peripheral immune tolerance, and regulating T-cell-mediated cytokine secretion. Unlike B7-1 and B7-2, PD-L1 has not been shown to influence immunity through interaction with CD28, CTL4A or ICOS, but rather through interaction with PD-1, a weak structural homolog of CTLA4 that belongs to the same superfamily. Involvement of PD-1 suggests an inhibitory function during T-cell activation; however, evidence has demonstrated PD-L1’s conflicting responsibility for both the stimulation and inhibition of T-cell-mediated cytokine synthesis. While T-cell co-stimulation with PD-L1 induces proliferation and the secretion of IL-10 and IFN-γ, muscle cell expression of PD-L1 has been shown to inhibit function of CD4 and CD8 T-cells by down-regulating cytokine secretion and the expression of T-cell activation markers. Augmented expression of PD-L1 has been linked to the inhibition of antitumor immune response in cancer, and the up-regulation of IL-10 production in HIV-infection, resulting in increased susceptibility of antigen-specific T-cells to apoptosis. PeproTech’s