CD279 (PD-1) Monoclonal Antibody (J116), Functional Grade, eBioscience™, Invitrogen™

Description

Description: The J116 monoclonal antibody reacts with the human PD-1 (programmed death-1), a 55 kDa member of the immunoglobulin superfamily. PD-1 contains the immunoreceptor tyrosine-based inhibitory motif (ITIM) and plays a key role in peripheral tolerance and autoimmune disease. PD-1 is expressed predomitly on activated T and B lymphocytes. Two novel members of the B7 family have been identified as the PD-1 ligands, PD-L1 (B7-H1) and PD-L2 (B7-DC). Evidence reported to date suggests overlapping functions for these two PD-1 ligands and their constitutive expression on some normal tissues and upregulation on activated antigen-presenting cells. Binding of the J116 monoclonal antibody inhibits PD-1 signal transduction, however, it does not block binding of the ligand PD-L1. Applications Reported: This J116 antibody has been reported in in vitro functional assays. Applications Tested: The J116 antibody has been tested by flow cytometric analysis of human PD-1 transfected cells. This can be used at less than or equal to 1 μg per test. A test is defined as the amount (μg) of antibody that will stain a cell sample in a final volume of 100 μL. Cell number should be determined empirically but can range from 10^5 to 10^8 cells/test. It is recommended that the antibody be carefully titrated for optimal performance in the assay of interest. Endotoxin: Less than 0.001 ng/ug antibody as determined by the LAL assay.

Cell-mediated immune responses are initiated by T lymphocytes that are themselves stimulated by cognate peptides bound to MHC molecules on antig en-presenting cells (APC). T-cell activation is generally self-limited as activated T cells express receptors such as PD-1 (also known as PDCD-1) that mediate inhibitory signals from the APC. PD-1 can bind two different but related ligands, PDL-1 and PDL-2. Upon binding to either of these ligands, signals generated by PD-1 inhibit the activation of the immune response in the absence of "e;danger signals"e; such as LPS or other molecules associated with bacteria or other pathogens. Evidence for this is seen in PD1-null mice who exhibit hyperactivated immune systems and autoimmune diseases. Despite its predicted molecular weight, PD-1 often migrates at higher molecular weight in SDS-PAGE.