Detection of PD‑1 in Mouse CD4+ T-Cells by Flow Cytometry.
Mouse CD4+ T-cells were stained with Goat Anti-Mouse PD‑1 PE‑conjugated Antigen Affinity-purified Polyclonal Antibody (Catalog # FAB1021P, filled histogram) or isotype control antibody (Catalog # IC108P, open histogram). View our protocol for Staining Membrane-associated Proteins.
Preparation and Storage
The product is shipped with polar packs. Upon receipt, store it immediately at the temperature recommended below.
Stability & Storage
Protect from light. Do not freeze.
12 months from date of receipt, 2 to 8 °C as supplied.
Programmed Death-1 (PD-1), also known as CD279, is type I transmembrane protein belonging to the CD28/CTLA-4 family of immunoreceptors that mediate signals for the regulation of immune responses (1). Other members of this family include CD28, BTLA, CTLA-4, and ICOS (2-4). PD-1 is most closely related to CTLA-4 and shares approximately 24% amino acid (aa) sequence identity. The mouse PD-1 gene encodes a 288 aa protein with a putative 20 aa signal peptide, a 149 aa extracellular region with one immunoglobulin-like V-type domain, a 21 aa transmembrane domain, and a 98 aa cytoplasmic region. The cytoplasmic tail contains two tyrosine residues that form the immunoreceptor tyrosine-based inhibitory motif (ITIM) and immunoreceptor tyrosine-based switch motif (ITSM) that are important in mediating PD-1 signaling. Mouse and human PD-1 share approximately 69% aa sequence identity. Two B7 family proteins, PD-L1 (also called B7-H1) and PD-L2, have been identified as PD-1 ligands (5, 6). PD-1 is expressed on activated T cells, B cells, myeloid cells, and on a subset of thymocytes. PD-1 deficient mice have a defect in peripheral tolerance and spontaneously develop autoimmune diseases. Binding of PD-1 to PD-L1 or PD-L2 results in the inhibition of TCR-mediated proliferation and cytokine production as well as BCR-mediated signaling. PD-1 likely plays an inhibitory role in the regulation of immune responses (1-4).
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Sharpe, A.H. and G.J. Freeman (2002) Nat. Rev. Immunol. 2:116.
Coyle, A. and J. Gutierrez-Ramos (2001) Nat. Immunol. 2:203.
Nishimura, H. and T. Honjo (2001) Trends Immunol. 22:265.
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