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$29.73 - $71.89

$29.73 - $71.89

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  • 100 µg - $71.89
  • 25 µg - $29.73
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Product Description

The 145-2C11 monoclonal antibody reacts with mouse CD3ε, a 20 kDa transmembrane cell-surface protein that belongs to the immunoglobulin superfamily. CD3ε is one of five polypeptide chains that combine to form the TCR complex. CD3ε is expressed on T lymphocytes, NK-T cells, and, to varying degrees, on developing thymocytes. CD3 plays roles in TCR signaling, T lymphocyte activation, and antigen recognition. The 145-2C11 antibody clone is well characterized, and its unique specificity for CD3ε makes it a reliable marker of T cells in experiments with mouse samples. This R-phycoerythrin (R-PE or PE)-conjugated version of the 145-2C11 antibody is useful for flow cytometry and immunofluorescence applications.

Specifications

Isotype Armenian Hamster IgG1
Conjugation PE
Excitation Source Yellow-Green 488 nm, 532 nm, 561 nm
Excitation Max 496 nm, 566 nm
Emission Max 576 nm
Immunogen Mouse BM10-37 cytotoxic T cells
Reported Applications Immunofluorescence
Flow cytometry
Formulation PBS, pH 7.0
Contains 0.09% Sodium Azide
Production Purified from cell culture supernatant in an animal-free facility
Purification Protein A. Conjugated with R-phycoerythrin under optimal conditions.
Storage The antibody solution should be stored at the stock concentration at 4°C and protected from prolonged exposure to light. Do not freeze.
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Application References

Immunofluorescence, in vitro T cell stimulation/activation, in vitro IL-4 neutralization
Kim, Y. U., et al. (2015). "Regulation of autoimmune germinal center reactions in lupus-prone BXD2 mice by follicular helper T cells" PLoS One 10(3): e0120294.
PubMed

BXD2 mice spontaneously develop autoantibodies and subsequent glomerulonephritis, offering a useful animal model to study autoimmune lupus. Although initial studies showed a critical contribution of IL-17 and Th17 cells in mediating autoimmune B cell responses in BXD2 mice, the role of follicular helper T (Tfh) cells remains incompletely understood. We found that both the frequency of Th17 cells and the levels of IL-17 in circulation in BXD2 mice were comparable to those of wild-type. By contrast, the frequency of PD-1+ CXCR5+ Tfh cells was significantly increased in BXD2 mice compared with wild-type mice, while the frequency of PD-1+ CXCR5+ Foxp3+ follicular regulatory T (Tfr) cells was reduced in the former group. The frequency of Tfh cells rather than that of Th17 cells was positively correlated with the frequency of germinal center B cells as well as the levels of autoantibodies to dsDNA. More importantly, CXCR5+ CD4+ T cells isolated from BXD2 mice induced the production of IgG from naive B cells in an IL-21-dependent manner, while CCR6+ CD4+ T cells failed to do so. These results together demonstrate that Tfh cells rather than Th17 cells contribute to the autoimmune germinal center reactions in BXD2 mice.

Flow Cytometry, in vitro T cell stimulation/activation, in vitro IL-4 neutralization, in vivo IL-12p40 neutralization, in vitro IL-12 p35 neutralization
Tang, W., et al. (2014). "The oncoprotein and transcriptional regulator Bcl-3 governs plasticity and pathogenicity of autoimmune T cells" Immunity 41(4): 555-566.
PubMed

Bcl-3 is an atypical member of the IkappaB family that modulates transcription in the nucleus via association with p50 (NF-kappaB1) or p52 (NF-kappaB2) homodimers. Despite evidence attesting to the overall physiologic importance of Bcl-3, little is known about its cell-specific functions or mechanisms. Here we demonstrate a T-cell-intrinsic function of Bcl-3 in autoimmunity. Bcl-3-deficient T cells failed to induce disease in T cell transfer-induced colitis and experimental autoimmune encephalomyelitis. The protection against disease correlated with a decrease in Th1 cells that produced the cytokines IFN-gamma and GM-CSF and an increase in Th17 cells. Although differentiation into Th1 cells was not impaired in the absence of Bcl-3, differentiated Th1 cells converted to less-pathogenic Th17-like cells, in part via mechanisms involving expression of the RORgammat transcription factor. Thus, Bcl-3 constrained Th1 cell plasticity and promoted pathogenicity by blocking conversion to Th17-like cells, revealing a unique type of regulation that shapes adaptive immunity.

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