Anti-Human PD-1 (CD279) [Clone J110] — CF®633

Human PD-1-Ig fusion protein

This CF®633 conjugate is formulated in 0.01 M phosphate buffered saline (150 mM NaCl) PBS pH 7.4, 1% BSA and 0.09% sodium azide as a preservative.

Liquid

This CF®633 conjugate is stable when stored at 2-8°C, protected from light. Do not freeze.

Research Use Only

2 – 8° C Wet Ice

633 nm or 635 nm

630/650 nm

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.