Anti-Human PD-1 (CD279) [Clone J110] — Purified in vivo GOLD™ Functional Grade

Human PD-1-Ig fusion protein

This monoclonal antibody is aseptically packaged and formulated in 0.01 M phosphate buffered saline (150 mM NaCl) PBS pH 7.2 - 7.4 with no carrier protein, potassium, calcium or preservatives added. Due to inherent biochemical properties of antibodies, certain products may be prone to precipitation over time. Precipitation may be removed by aseptic centrifugation and/or filtration.

Liquid

Functional grade preclinical antibodies are manufactured in an animal free facility using only in vitro protein free cell culture techniques and are purified by a multi-step process including the use of protein A or G to assure extremely low levels of endotoxins, leachable protein A or aggregates.

Functional grade preclinical antibodies may be stored sterile as received at 2-8°C for up to one month. For longer term storage, aseptically aliquot in working volumes without diluting and store at ≤ -70°C. Avoid Repeated Freeze Thaw Cycles.

Research Use Only

2 – 8° C Wet Ice

Activity is directed against the extracellular domain of human Programmed Cell Death 1 (PD-1), also known as CD279. Clone J110 recognizes the native surface receptor on activated T cells, B cells, and myeloid cells.

Programmed Cell Death 1 (PD-1/CD279) is a 50–55 kDa transmembrane glycoprotein belonging to the CD28 family of the immunoglobulin superfamily. It functions as a critical immune checkpoint receptor that maintains peripheral tolerance and prevents autoimmunity². Under normal physiological conditions, PD-1 expression is transiently induced following antigen receptor signaling. However, in contexts of chronic antigen exposure (such as cancer or chronic viral infection), PD-1 expression becomes sustained, marking a state of T cell dysfunction known as "exhaustion"³.

PD-1 interacts with two ligands: PD-L1 (B7-H1/CD274) and PD-L2 (B7-DC/CD273). Ligand binding triggers the phosphorylation of the Immunoreceptor Tyrosine-based Inhibitory Motif (ITIM) and the Immunoreceptor Tyrosine-based Switch Motif (ITSM) within the PD-1 cytoplasmic tail⁴. These phosphorylated motifs recruit the protein tyrosine phosphatases SHP-1 and SHP-2, which dephosphorylate downstream effector molecules (such as ZAP70 and PI3K), thereby inhibiting T cell proliferation, cytokine production (IL-2, IFN-γ), and cytotoxic activity⁵.

Clone J110 is a widely used monoclonal antibody for the flow cytometric detection of PD-1. Unlike some therapeutic clones that are designed specifically to block the PD-1/PD-L1 interaction for clinical immunotherapy, J110 is frequently utilized in research to phenotype immune cells and assess the activation status of lymphocytes in peripheral blood and tissue samples¹. High levels of PD-1 detected by clones such as J110 are often correlated with reduced effector function and poor viral control in diseases like HIV and Hepatitis C⁶.

PD-1 is an inducible surface receptor expressed primarily on activated CD4+ and CD8+ T cells, B cells, Natural Killer (NK) cells, monocytes, and dendritic cells. It is a marker of "exhausted" T cells in chronic viral infections and the tumor microenvironment¹.

Receptor: PD-1 / Ligands: PD-L1 (B7-H1), PD-L2 (B7-DC)

1. Keir ME, Butte MJ, Freeman GJ, Sharpe AH. PD-1 and its ligands in tolerance and immunity. Annu Rev Immunol. 26:677-704. 2008.
2. Ishida Y, Agata Y, Shibahara K, Honjo T. Induced expression of PD-1, a novel member of the immunoglobulin gene superfamily, upon programmed cell death. EMBO J. 11(11):3887-3895. 1992.
3. Wherry EJ. T cell exhaustion. Nat Immunol. 12(6):492-499. 2011.
4. Parry RV, Chemnitz JM, Frauwirth KA, et al. CTLA-4 and PD-1 receptors inhibit T-cell activation by distinct mechanisms. Mol Cell Biol. 25(21):9543-9553. 2005.
5. Freeman GJ, Long AJ, Iwai Y, et al. Engagement of the PD-1 immunoinhibitory receptor by a novel B7 family member leads to negative regulation of lymphocyte activation. J Exp Med. 192(7):1027-1034. 2000.
6. Day CL, Kaufmann DE, Kiepiela P, et al. PD-1 expression on HIV-specific T cells is associated with T-cell exhaustion and disease progression. Nature. 443(7109):350-354. 2006.