Recombinant Human PD-L2 (B7-DC, CD273)-Fc Chimera (carrier-free)
Description
PD-L2 is a type I transmembrane protein of 273 amino acids, and it is a member of the B7 family. Human PD-L2 has 70% amino acid identity to its mouse orthologue. PD-L2 is the second ligand for PD-1, and its binding to PD-1 leads to the inhibition of T cell receptor–mediated lymphocyte proliferation and cytokine secretion. PD-L2/PD-1 interaction suppresses immune responses against autoantigens and tumors and plays an important role in the maintenance of peripheral immune tolerance. Antibody blocking of PD-L2 on dendritic cells results in enhanced T cell proliferation and cytokine production. Interaction of PD-1 by PD-L1-Ig or PD-L2-Ig fusion protein has an inhibitory effect on proliferation and cytokine production during anti-CD3-mediated stimulation. PD-L2 is expressed in biopsies from human asthmatics and lungs of aeroallergen-treated mice and its expression correlates with the asthma severity. In vivo blockade of PD-L2 reduces the severity of allergen-driven airway hyperresponsiveness (AHR).? Blockage of PD-L2 induces the IL-12 production by DC; IL-12 may limit the severity of allergen-induced AHR antagonizing IL-13. In addition, blockade of PD-1 does not have effect on AHR; therefore, PD-L2 controls asthma severity in a PD-1 independent manner. PD-L2 binds to a second receptor, RGMb (repulsive guidance molecule b) which is expressed in lung interstitial macrophages and alveolar epithelial cells and is a co-receptor for bone morphogenetic proteins BMP2/4. Blockade of the RGMb/PD-L2 interaction significantly impaired the development of respiratory tolerance since the initial T cell expansion is inhibited.