Human LAG-3 Biotinylated Antibody Summary
Leu23-Leu450
Accession # P18627
Applications
Please Note: Optimal dilutions should be determined by each laboratory for each application. General Protocols are available in the Technical Information section on our website.
Scientific Data
Detection of LAG‑3 in CD3+Human PBMCs by Flow Cytometry. CD3+Human peripheral blood mononuclear cells (PBMCs) treated with 5 µg/mL PHA for 5 days were stained with Mouse Anti-Human CD3e PE-conjugated Monoclonal Antibody (Catalog # FAB100P) and either (A) Goat Anti-Human LAG-3 Biotinylated Antigen Affinity-purified Polyclonal Antibody (Catalog # BAF2319) or (B) Normal Goat IgG Biotinylated Control (Catalog # BAF108) followed by Streptavidin-Allophycocyanin (Catalog # F0050).
Reconstitution Calculator
Preparation and Storage
- 12 months from date of receipt, -20 to -70 °C as supplied.
- 1 month, 2 to 8 °C under sterile conditions after reconstitution.
- 6 months, -20 to -70 °C under sterile conditions after reconstitution.
Background: LAG-3
LAG-3 (Lymphocyte activation gene-3), also known as CD223, is a member of the immunoglobulin superfamily (IgSF). The mature LAG-3 protein is a 496 amino acid (aa) membrane protein with a 421 aa extracellular region which contains four IgSF domains, a 21 aa transmembrane region and a 54 aa cytoplasmic region. LAG-3 and CD4 molecules share < 20% aa sequence homology but have a similar structure (1, 2). Both molecules bind to MHC class II. LAG-3 binds to MHC class II with higher affinity compared to CD4. Both LAG-3 and CD4 genes are located on the distal part of the short arm of chromosome 12.
LAG-3 is an activation-induced molecule, expressed on activated T cells and NK cells, but not on resting T cells. Studies using LAG-3 -/- mice have shown significant delay of T cell apoptosis following antigen stimulation and increased size of memory T cells pool following infection (3, 4). It also has been reported that anti-LAG-3 antibodies up-regulate T cell activation by blocking interaction of LAG-3 and MHC class II. The study has demonstrated that LAG-3 is selectively expressed on activated CD4+CD25+ TReg cells and plays a role in their suppressive activity (5). This evidence indicated, unlike the interaction of CD4 with MHC class II that plays a positive role in T cell activation, LAG-3 binds to MHC class II and negatively regulates T cell activation through LAG-3 signaling. On the other hand, studies have shown that binding of LAG-3 to MHC class II molecules on antigen presenting cells induce maturation of dendritic cells and cytokine secretion by monocytes through MHC class II signal transduction (6). Taken together, LAG-3 may have two major functions, it negatively regulates T cells activation through LAG-3 signaling and stimulates antigen presenting cells which express MHC class II.
- Triebel, F. et al. (1990) J. Exp. Med. 171:1393.
- Baixeras, E. et al. (1992) J. Exp. Med 176:327.
- Workman, C.J. and D.A. Vignali (2003) Eur. J. Immunol. 33:970.
- Workman, C.J. et al. (2004) J. Immunol. 172:5450.
- Huang, C.T. et al. (2004) Immunity 21:503.
- Andreae, S. et al. (2003) Blood 102:2130.
Product Datasheets
Citations for Human LAG-3 Biotinylated Antibody
R&D Systems personnel manually curate a database that contains references using R&D Systems products. The data collected includes not only links to publications in PubMed, but also provides information about sample types, species, and experimental conditions.
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Chronic exposure to Plasmodium falciparum is associated with phenotypic evidence of B and T cell exhaustion.
Authors: Illingworth, Joseph, Butler, Noah S, Roetynck, Sophie, Mwacharo, Jedida, Pierce, Susan K, Bejon, Philip, Crompton, Peter D, Marsh, Kevin, Ndungu, Francis
J Immunol, 2012-12-21;190(3):1038-47.
Species: Human
Sample Types: Whole Cells
Applications: Flow Cytometry -
Expansion of interferon-gamma-producing multifunctional CD4+ T-cells and dysfunctional CD8+ T-cells by glypican-3 peptide library in hepatocellular carcinoma patients☆
Authors: Yanhui Xu, Hong Li, Rui Lin Gao, Oluwasayo Adeyemo, Maxim Itkin, David E. Kaplan
Clinical Immunology
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