InVivoMAb anti-mouse CD25 (IL-2Rα)
Product Description
Specifications
| Isotype | Rat IgG1, λ |
|---|---|
| Recommended Isotype Control(s) | InVivoMAb rat IgG1 isotype control, anti-horseradish peroxidase |
| Recommended Dilution Buffer | InVivoPure pH 7.0 Dilution Buffer |
| Conjugation | This product is unconjugated. Conjugation is available via our Antibody Conjugation Services. |
| Immunogen | IL-2-dependent cytolytic mouse T cell clone B6.1 |
| Reported Applications |
in vivo regulatory T cell depletion Flow cytometry |
| Formulation |
PBS, pH 7.0 Contains no stabilizers or preservatives |
| Endotoxin |
≤1EU/mg (≤0.001EU/μg) Determined by LAL assay |
| Purity |
≥95% Determined by SDS-PAGE |
| Sterility | 0.2 µm filtration |
| Production | Purified from cell culture supernatant in an animal-free facility |
| Purification | Protein A High Salt |
| RRID | AB_1107619 |
| Molecular Weight | 150 kDa |
| Storage | The antibody solution should be stored at the stock concentration at 4°C. Do not freeze. |
| Need a Custom Formulation? | See All Antibody Customization Options |
Application References
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Miller, M. L., et al (2015). "Spontaneous restoration of transplantation tolerance after acute rejection" Nat Commun 6: 7566.
PubMed
Transplantation is a cure for end-stage organ failure but, in the absence of pharmacological immunosuppression, allogeneic organs are acutely rejected. Such rejection invariably results in allosensitization and accelerated rejection of secondary donor-matched grafts. Transplantation tolerance can be induced in animals and a subset of humans, and enables long-term acceptance of allografts without maintenance immunosuppression. However, graft rejection can occur long after a state of transplantation tolerance has been acquired. When such an allograft is rejected, it has been assumed that the same rules of allosensitization apply as to non-tolerant hosts and that immunological tolerance is permanently lost. Using a mouse model of cardiac transplantation, we show that when Listeria monocytogenes infection precipitates acute rejection, thus abrogating transplantation tolerance, the donor-specific tolerant state re-emerges, allowing spontaneous acceptance of a donor-matched second transplant. These data demonstrate a setting in which the memory of allograft tolerance dominates over the memory of transplant rejection.
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Christensen, A. D., et al (2015). "Depletion of regulatory T cells in a hapten-induced inflammation model results in prolonged and increased inflammation driven by T cells" Clin Exp Immunol 179(3): 485-499.
PubMed
Regulatory T cells (Tregs ) are known to play an immunosuppressive role in the response of contact hypersensitivity (CHS), but neither the dynamics of Tregs during the CHS response nor the exaggerated inflammatory response after depletion of Tregs has been characterized in detail. In this study we show that the number of Tregs in the challenged tissue peak at the same time as the ear-swelling reaches its maximum on day 1 after challenge, whereas the number of Tregs in the draining lymph nodes peaks at day 2. As expected, depletion of Tregs by injection of a monoclonal antibody to CD25 prior to sensitization led to a prolonged and sustained inflammatory response which was dependent upon CD8 T cells, and co-stimulatory blockade with cytotoxic T lymphocyte antigen-4-immunoglobulin (CTLA-4-Ig) suppressed the exaggerated inflammation. In contrast, blockade of the interleukin (IL)-10-receptor (IL-10R) did not further increase the exaggerated inflammatory response in the Treg -depleted mice. In the absence of Tregs , the response changed from a mainly acute reaction with heavy infiltration of neutrophils to a sustained response with more chronic characteristics (fewer neutrophils and dominated by macrophages). Furthermore, depletion of Tregs enhanced the release of cytokines and chemokines locally in the inflamed ear and augmented serum levels of the systemic inflammatory mediators serum amyloid (SAP) and haptoglobin early in the response.
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Richter, K., et al (2013). "Macrophage and T cell produced IL-10 promotes viral chronicity" PLoS Pathog 9(11): e1003735.
PubMed
Chronic viral infections lead to CD8(+) T cell exhaustion, characterized by impaired cytokine secretion. Presence of the immune-regulatory cytokine IL-10 promotes chronicity of Lymphocytic Choriomeningitis Virus (LCMV) Clone 13 infection, while absence of IL-10/IL-10R signaling early during infection results in viral clearance and higher percentages and numbers of antiviral, cytokine producing T cells. IL-10 is produced by several cell types during LCMV infection but it is currently unclear which cellular sources are responsible for induction of viral chronicity. Here, we demonstrate that although dendritic cells produce IL-10 and overall IL-10 mRNA levels decrease significantly in absence of CD11c(+) cells, absence of IL-10 produced by CD11c(+) cells failed to improve the LCMV-specific T cell response and control of LCMV infection. Similarly, NK cell specific IL-10 deficiency had no positive impact on the LCMV-specific T cell response or viral control, even though high percentages of NK cells produced IL-10 at early time points after infection. Interestingly, we found markedly improved T cell responses and clearance of normally chronic LCMV Clone 13 infection when either myeloid cells or T cells lacked IL-10 production and mice depleted of monocytes/macrophages or CD4(+) T cells exhibited reduced overall levels of IL-10 mRNA. These data suggest that the decision whether LCMV infection becomes chronic or can be cleared critically depends on early CD4(+) T cell and monocyte/macrophage produced IL-10.
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Goschl, L., et al (2018). "A T cell-specific deletion of HDAC1 protects against experimental autoimmune encephalomyelitis" J Autoimmun 86: 51-61.
PubMed
Multiple sclerosis (MS) is a human neurodegenerative disease characterized by the invasion of autoreactive T cells from the periphery into the CNS. Application of pan-histone deacetylase inhibitors (HDACi) ameliorates experimental autoimmune encephalomyelitis (EAE), an animal model for MS, suggesting that HDACi might be a potential therapeutic strategy for MS. However, the function of individual HDAC members in the pathogenesis of EAE is not known. In this study we report that mice with a T cell-specific deletion of HDAC1 (using the Cd4-Cre deleter strain; HDAC1-cKO) were completely resistant to EAE despite the ability of HDAC1cKO CD4(+) T cells to differentiate into Th17 cells. RNA sequencing revealed STAT1 as a prominent upstream regulator of differentially expressed genes in activated HDAC1-cKO CD4(+) T cells and this was accompanied by a strong increase in phosphorylated STAT1 (pSTAT1). This suggests that HDAC1 controls STAT1 activity in activated CD4(+) T cells. Increased pSTAT1 levels correlated with a reduced expression of the chemokine receptors Ccr4 and Ccr6, which are important for the migration of T cells into the CNS. Finally, EAE susceptibility was restored in WT:HDAC1-cKO mixed BM chimeric mice, indicating a cell-autonomous defect. Our data demonstrate a novel pathophysiological role for HDAC1 in EAE and provide evidence that selective inhibition of HDAC1 might be a promising strategy for the treatment of MS.
Product Citations
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Antigen choice determines vaccine-induced generation of immunogenic versus tolerogenic dendritic cells that are marked by differential expression of pancreatic enzymes.
In The Journal of Immunology on 1 April 2013 by Farkas, A. M., Marvel, D. M., et al.
PubMed
Dendritic cells (DC) elicit immunity to pathogens and tumors while simultaneously preserving tolerance to self. Efficacious cancer vaccines have been a challenge because they are based on tumor Ags, some of which are self-Ags and thus subject to self-tolerance. One such Ag is the tumor-associated mucin MUC1. Preclinical testing of MUC1 vaccines revealed existence of peripheral tolerance to MUC1 that compromises their efficacy. To identify mechanisms that act early postvaccination and might predict vaccine outcome, we immunized human MUC1 transgenic mice (MUC1.Tg) i.v. with a MUC1 peptide vaccine against which they generate weak immunity and wild-type (WT) mice that respond strongly to the same peptide. We analyzed differences in splenic DC phenotype and function between the two mouse strains at 24 and 72 h postvaccination and also performed unbiased total gene expression analysis of the spleen. Compared to WT, MUC1.Tg spleens had significantly fewer DC, and they exhibited significantly lower expression of costimulatory molecules, decreased motility, and preferential priming of Ag-specific Foxp3(+) regulatory T cells. This tolerogenic DC phenotype and function was marked by a new putative biomarker revealed by the microarray: a cohort of pancreatic enzymes (trypsin, carboxypeptidase, elastase, and others) not previously reported in DC. These enzymes were strongly upregulated in the splenic DC from vaccinated WT mice and suppressed in the splenic DC of vaccinated MUC1.Tg mice. Suppression of the enzymes was dependent on regulatory T cells and on signaling through the IL-10R and correlated with global downregulation of DC immunostimulatory phenotype and function.
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Colonic Engyodontium fungus triggers neutrophil antimicrobial activity to suppress Lactobacillus johnsonii-derived glutamic acid-maintained Tregs.
In J Clin Invest on 15 April 2026 by Wang, X., Sun, H., et al.
PubMed
Isolating commensal fungi from mouse intestines has been challenging, limiting our understanding of their role in intestinal immune homeostasis and diseases. Using an Fc fusion protein of the C-type lectin receptor Dectin-2, we successfully purified the commensal Ascomycota fungus Engyodontium sp. from mouse feces. Engyodontium enhances the antimicrobial activity of colonic neutrophils via the CARD9 pathway and exacerbates colitis by impairing the colonization of intestinal Lactobacillus johnsonii WXY strain. L. johnsonii produces high levels of l-glutamic acid by expressing the glutaminase-encoding gene glsA to facilitate Treg expansion via enhancing IL-2 receptor signaling. Patients with Crohn disease (CD) and ulcerative colitis harbored increased Engyodontium and decreased L. johnsonii abundance. Engyodontium directly induced calprotectin in human colonic neutrophils, and patients with CD had lower levels of l-glutamic acid, which also promoted human Treg expansion. These findings highlight the Engyodontium-calprotectin axis against the Lactobacillus-glutamate-Treg cascade to aggravate colitis, suggesting commensal Engyodontium-triggered signaling as a therapeutic target for mucosal inflammatory diseases.
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CD25 modulation enhances broadly neutralizing antibody response of SARS-CoV-2 subunit vaccine.
In Commun Biol on 17 February 2026 by Li, F., Yu, X., et al.
PubMed
The primary aim of COVID-19 vaccine development is to induce highly efficient broadly neutralizing antibodies (bNAbs) against circulating and emergent SARS-CoV-2 variants. Rapid and sustained germinal center (GC) responses at an early stage are crucial to produce bNAbs. However, the mechanisms underlying the formation of early GC responses and strategies to effectively promote these responses remain to be further investigated. In this study, we found that the combination of anti-CD25 monoclonal antibodies (mAb) with the COVID-19 subunit vaccine significantly enhances cross-reactive neutralizing antibody responses in mice. Modulation of CD25 at different time points before and after vaccination resulted in varying effects on the GC response, with day 0 being the most effective in assisting the vaccine to induce a stronger GC response. This enhancement is achieved by rapidly inhibiting regulatory T (Treg) cells in draining lymph nodes, an effect observed not only in antigen-specific subsets but also across the bulk lymphocyte population-thereby creating a pro-immune microenvironment that facilitates the induction of an effective early GC response. This leads to the generation of more antigen-recognizing B cells and significantly increases both the potency and breadth of neutralizing antibody responses. Our findings propose a strategy to enhance vaccine efficacy against SARS-CoV-2 and other hypervariable pathogens by effectively promoting the development of early and robust GC responses.
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A CD25-chemokine receptor complex initiates noncanonical IL-2 signaling.
In J Biol Chem on 1 January 2026 by Lee, H., Kim, S. H. J., et al.
PubMed
An antimouse CD25 antibody, PC61, induces a complex formed by the interleukin-2 (IL-2)-dependent association of CD25 with CCR7 and an alternative IL-2 signaling pathway that results in integrin activation in CD4+CD25HiFoxp3+ regulatory T cells (Tregs). Here, we used structure-based design together with combinatorial screening to identify a human IL-2 mutant (IL-2(E52K)) that disrupts CD25-CCR7 complex formation while retaining the full CD25 affinity of the parent molecule. An anti-human CD25 (hCD25), 7G7B6, drove formation of IL-2-dependent hCD25-CCR7, CD25-CXCR4, and CD25-CCR5 complexes and induced integrin activation in hCD25-expressing IL-2Rα+ YT-1 cells, Jurkat T cells, and primary Tregs. IL-2(E52K) failed to support activation in CCR5Lo Jurkat T cells and primary Tregs. In contrast, IL-2(E52K) supported activation in CCR5Hi IL-2Rα+ YT-1 cells, which was blocked by the CCR5-specific antagonist, maraviroc. Heparan sulfate (HS), a physiological ligand of IL-2, induced IL-2-dependent CD25-CCR7 association, and IL-2(E52K) failed to support HS-induced CD25-CCR7 complex formation and integrin activation in Jurkat cells. Both HS and 7G7B6 did not block canonical IL-2 signaling. CD122 was present in the 7G7B6-induced CCR7-CD25 complex. CD122 forms a heterodimer with CD132 (the common γ chain) that triggers canonical IL-2 signaling. Thus, both anti-CD25 antibody and HS require formation of a chemokine receptor-CD25 complex to initiate alternative IL-2 signaling. In addition, our findings suggest that alternative and canonical IL-2 signaling receptors can be incorporated into the same multiprotein assembly, allowing for a single complex to mediate divergent effects on downstream signaling.