CD279 (PD-1) Monoclonal Antibody (J116), 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 for use in immunoprecipitation and immunohistology staining of frozen tissue sections. It has also been reported in in vitro functional assays. (Please use Functional Grade purified J116, cat. 16-9989, in 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.

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.