InVivoMAb anti-mouse CD25 (IL-2Rα)

Clone Catalog # Category
7D4 BE0013 InVivoMab Antibodies
$95 - $3250

About InVivoMAb anti-mouse CD25 (IL-2Rα)

The 7D4 monoclonal antibody reacts with mouse IL-2Rα also known as CD25, Ly-43, p55, or Tac. IL-2Rα is the 55 kDa ligand-binding subunit of the interleukin 2 receptor alpha chain. IL-2Rα is expressed on activated mature T and B lymphocytes, thymocyte subsets, pre-B cells, and T regulatory cells. IL-2Rα has been shown to play roles in lymphocyte differentiation, activation, and proliferation. Alone, the IL-2Rα binds IL-2 with relatively low affinity however, when IL-2Rα associates with IL-2Rβ (CD122) and the common gamma chain (CD132) the complex binds IL-2 with high affinity. The 7D4 antibody recognizes a different epitope on CD25 than the PC-61.5.3 clone.

InVivoMAb anti-mouse CD25 (IL-2Rα) Specifications

Isotype

Rat IgM, κ

Recommended Isotype Control(s) InVivoMAb polyclonal rat IgG(BE0094)
Recommended InVivoPure Dilution Buffer InVivoPure pH 7.0 Dilution Buffer(IP0070)
Immunogen

IL-2-dependent BALB/c mouse T cell clone HT2

Reported Applications

in vivo regulatory T cell inactivation

Endotoxin
  • <2EU/mg (<0.002EU/μg)
  • Determined by LAL gel clotting assay
Purity
  • >95%
  • Determined by SDS-PAGE
Formulation
  • PBS, pH 7.0
  • Contains no stabilizers or preservatives
Sterility

0.2 μM filtered

Production

Purified from tissue culture supernatant in an animal free facility

Purification

T-Gel

Storage

The antibody solution should be stored undiluted at 4°C, and protected from prolonged exposure to light. Do not freeze.

RRID

AB_1107615

Application References

InVivoMAb anti-mouse CD25 (IL-2Rα) (Clone: 7D4)

  Podojil, J. R., et al. (2013). "B7-H4Ig inhibits mouse and human T-cell function and treats EAE via IL-10/Treg-dependent mechanisms." J Autoimmun 44: 71-81. PubMed

We evaluated the therapeutic efficacy and mechanisms of action of both mouse and human B7-H4 Immunoglobulin fusion proteins (mB7-H4Ig; hB7-H4Ig) in treating EAE. The present data show that mB7-H4Ig both directly and indirectly (via increasing Treg function) inhibited CD4(+) T-cell proliferation and differentiation in both Th1- and Th17-cell promoting conditions while inducing production of IL-10. B7-H4Ig treatment effectively ameliorated progression of both relapsing (R-EAE) and chronic EAE correlating with decreased numbers of activated CD4(+) T-cells within the CNS and spleen, and a concurrent increase in number and function of Tregs. The functional requirement for Treg activation in treating EAE was demonstrated by a loss of therapeutic efficacy of hB7-H4Ig in R-EAE following inactivation of Treg function either by anti-CD25 treatment or blockade of IL-10. Significant to the eventual translation of this treatment into clinical practice, hB7-H4Ig similarly inhibited the in vitro differentiation of naive human CD4(+) T-cells in both Th1- and Th17-promoting conditions, while promoting the production of IL-10. B7-H4Ig thus regulates pro-inflammatory T-cell responses by a unique dual mechanism of action and demonstrates significant promise as a therapeutic for autoimmune diseases, including MS.

Frimpong-Boateng, K., et al. (2010). "Regulatory T cells suppress natural killer cells during plasmid DNA vaccination in mice, blunting the CD8+ T cell immune response by the cytokine TGFbeta." PLoS One 5(8): e12281. PubMed

BACKGROUND: CD4(+)CD25(+) regulatory T cells (Tregs) suppress adaptive T cell-mediated immune responses to self- and foreign-antigens. Tregs may also suppress early innate immune responses to vaccine antigens and might decrease vaccine efficacy. NK and NKT cells are the first responders after plasmid DNA vaccination and are found at the site of inoculation. Earlier reports demonstrated that NKT cells could improve plasmid DNA efficacy, a phenomenon not found for NK cells. In fact, it has been shown that under certain disease conditions, NK cells are suppressed by Tregs via their release of IL-10 and/or TGFbeta. Therefore, we tested the hypothesis that NK cell function is suppressed by Tregs in the setting of plasmid DNA vaccination. METHODOLOGY/PRINCIPAL FINDINGS: In this study we show that Tregs directly inhibit NK cell function during plasmid DNA vaccination by suppressing the potentially 10-fold, NK cell-mediated, augmentation of plasmid DNA antigen-specific CD8(+) T cells. We found that this phenomenon is dependent on the secretion of cytokine TGFbeta by Tregs, and independent of IL-10. CONCLUSIONS: Our data indicate a crucial function for Tregs in blocking plasmid DNA vaccine-elicited immune responses, revealing potentially novel strategies for improving the efficiency of plasmid DNA vaccines including chemical- or antibody-induced localized blockage of Treg-mediated suppression of NK cells at the site of plasmid DNA vaccine inoculation.

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