Mouse KLRG1 PE-conjugated Antibody
Mouse KLRG1 PE-conjugated Antibody Summary
Glu57-Tyr188
Accession # O88713
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
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Detection of KLRG1 in Mouse Splenocytes by Flow Cytometry. Mouse splenocytes were stained with Mouse Anti-Mouse CD161/NK1.1 APC-conjugated Monoclonal Antibody (Catalog # FAB8319A) and either (A) Rabbit Anti-Mouse KLRG1 PE-conjugated Monoclonal Antibody (Catalog # FAB6944P) or (B) Normal Rabbit IgG Phycoerythrin Control (Catalog # IC105P). View our protocol for Staining Membrane-associated Proteins.
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Preparation and Storage
- 12 months from date of receipt, 2 to 8 °C as supplied.
Background: KLRG1
KLRG1 (Killer cell Lectin-like Receptor G1), also called MAFA (Mast cell Function Associated), is an inhibitory type II transmembrane glycoprotein of the C-type lectin family, designated CLEC15A (1). Mature mouse KLRG1 consists of a 33 amino acid (aa) cytoplasmic domain with one Immunoreceptor Tyrosine-based Inhibitory Motif (ITIM), a 23 aa transmembrane segment, and a 132 aa extracellular domain (ECD) with one C-type lectin domain (CTLD) (2). Within the ECD, mouse KLRG1 shares 57% and 80% aa sequence identity with human and rat KLRG1, respectively. Alternate splicing generates additional isoforms of mouse KLRG1 that lack either the CTLD or the CTLD, transmembrane segment, and a portion of the cytoplasmic domain (3). KLRG1 is expressed as a 30-40 kDa N-glycosylated molecule that forms disulfide-linked homodimers, trimers, and tetramers (4, 5). It is expressed on subpopulations of CD8+, CD4+, regulatory, and gamma/delta T cells as well as on NK cells (2, 4, 6-8). KLRG1 is expressed on T cells found in cord blood, but it is down-regulated postnatally and is subsequently re-expressed on antigen-exposed T cells (7, 9). It is expressed by a greater proportion of CD8+ T cells in the elderly and by virus-specific CD8+ T cells during chronic virus infection (10-12). KLRG1 binds to E-, N-, and R-Cadherins, triggering ITIM-dependent KLRG1 signaling and inhibition of T cell activation (5, 13, 14). The response is bi‑directional, as KLRG1 binding to E-Cadherin on dendritic cells (DC) can induce an anti-inflammatory DC phenotype (increased IL-10 production and decreased IL-6 and TNF-alpha production) (15).
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- Rosshart, S. et al. (2008) Eur. J. Immunol. 38:3354.
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- Beyersdorf, N. et al. (2007) Eur. J. Immunol. 37:3445.
- Eberl, M. et al. (2005) J. Leukoc. Biol. 77:67.
- Marcolino, I. et al. (2004) Eur. J. Immunol. 34:2672.
- Ouyang, Q. et al. (2003) Exp. Gerontol. 38:911.
- Thimme, R. et al. (2005) J. Virol. 79:12112.
- Cush, S.S. and E. Flano (2011) J. Immunol. 186:4051.
- Ito, M. et al. (2006) J. Exp. Med. 203:289.
- Tessmer, M.S. et al. (2007) Int. Immunol. 19:391.
- Banh, C. et al. (2009) Blood 114:5299.
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