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InVivoPlus anti-mouse PD-1 (CD279)

Research Use Only
BP0273
Bio X Cell
ApplicationsFlow Cytometry, ImmunoFluorescence, Western Blot, ImmunoHistoChemistry, ImmunoHistoChemistry Frozen, Neutralisation/Blocking
Product group Antibodies
ReactivityMouse
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Overview

  • Supplier
    Bio X Cell
  • Product Name
    InVivoPlus anti-mouse PD-1 (CD279)
  • Delivery Days Customer
    7
  • Applications
    Flow Cytometry, ImmunoFluorescence, Western Blot, ImmunoHistoChemistry, ImmunoHistoChemistry Frozen, Neutralisation/Blocking
  • Certification
    Research Use Only
  • Clonality
    Monoclonal
  • Clone ID
    29F.1A12™
  • Concentration
    4-11 mg/ml
  • Host
    Rat
  • Isotype
    IgG2a
  • Scientific Description
    The 29F.1A12™ monoclonal antibody reacts with mouse PD-1 (programmed death-1) also known as CD279. PD-1 is a 50-55 kDa cell surface receptor encoded by the Pdcd1 gene that belongs to the CD28 family of the Ig superfamily. PD-1 is transiently expressed on CD4 and CD8 thymocytes as well as activated T and B lymphocytes and myeloid cells. PD-1 expression declines after successful elimination of antigen. Additionally, Pdcd1 mRNA is expressed in developing B lymphocytes during the pro-B-cell stage. PD-1’s structure includes a ITIM (immunoreceptor tyrosine-based inhibitory motif) suggesting that PD-1 negatively regulates TCR signals. PD-1 signals via binding its two ligands, PD-L1 and PD-L2 both members of the B7 family. Upon ligand binding, PD-1 signaling inhibits T-cell activation, leading to reduced proliferation, cytokine production, and T-cell death. Additionally, PD-1 is known to play key roles in peripheral tolerance and prevention of autoimmune disease in mice as PD-1 knockout animals show dilated cardiomyopathy, splenomegaly, and loss of peripheral tolerance. Induced PD-L1 expression is common in many tumors including squamous cell carcinoma, colon adenocarcinoma, and breast adenocarcinoma. PD-L1 overexpression results in increased resistance of tumor cells to CD8 T cell mediated lysis. In mouse models of melanoma, tumor growth can be transiently arrested via treatment with antibodies which block the interaction between PD-L1 and its receptor PD-1. For these reasons anti-PD-1 mediated immunotherapies are currently being explored as cancer treatments. Like the RMP1-14 and J43 antibodies the 29F.1A12™ antibody has been shown to block the binding of PD-1 to its ligands in vivo.
  • Reactivity
    Mouse
  • Storage Instruction
    2°C to 8°C
  • UNSPSC
    12352203

References

  • RIP1 Kinase Drives Macrophage-Mediated Adaptive Immune Tolerance in Pancreatic Cancer. Wang W et al., 2018 Nov 12, Cancer Cell
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  • PD-1 expression by tumour-associated macrophages inhibits phagocytosis and tumour immunity. Gordon SR et al., 2017 May 25, Nature
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  • Adaptive resistance to therapeutic PD-1 blockade is associated with upregulation of alternative immune checkpoints. Koyama S et al., 2016 Feb 17, Nat Commun
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  • STK11/LKB1 Deficiency Promotes Neutrophil Recruitment and Proinflammatory Cytokine Production to Suppress T-cell Activity in the Lung Tumor Microenvironment. Koyama S et al., 2016 Mar 1, Cancer Res
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  • Response to BRAF inhibition in melanoma is enhanced when combined with immune checkpoint blockade. Cooper ZA et al., 2014 Jul, Cancer Immunol Res
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  • Negative role of inducible PD-1 on survival of activated dendritic cells. Park SJ et al., 2014 Apr, J Leukoc Biol
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  • Dual blockade of PD-1 and CTLA-4 combined with tumor vaccine effectively restores T-cell rejection function in tumors. Duraiswamy J et al., 2013 Jun 15, Cancer Res
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  • CD80 expression on B cells regulates murine T follicular helper development, germinal center B cell survival, and plasma cell generation. Good-Jacobson KL et al., 2012 May 1, J Immunol
    Read more
  • Role of the immune modulator programmed cell death-1 during development and apoptosis of mouse retinal ganglion cells. Chen L et al., 2009 Oct, Invest Ophthalmol Vis Sci
    Read more
  • Programmed death 1 ligand (PD-L) 1 and PD-L2 limit autoimmune kidney disease: distinct roles. Menke J et al., 2007 Dec 1, J Immunol
    Read more

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