InVivoMAb anti-mouse IL-12 p40
Product Description
Specifications
| Isotype | Rat IgG2a, κ |
|---|---|
| Recommended Isotype Control(s) | InVivoMAb rat IgG2a isotype control, anti-trinitrophenol |
| Recommended Dilution Buffer | InVivoPure pH 7.0 Dilution Buffer |
| Conjugation | This product is unconjugated. Conjugation is available via our Antibody Conjugation Services. |
| Immunogen | Recombinant mouse IL-12 p70 |
| Reported Applications |
in vivo IL-12p40 neutralization p40 affinity chromatography Immunoprecipitation ELISA Flow cytometry Western blot |
| 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 G |
| RRID | AB_1107698 |
| 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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Dann, S. M., et al (2018). "Giardia Infection of the Small Intestine Induces Chronic Colitis in Genetically Susceptible Hosts" J Immunol 201(2): 548-559.
PubMed
Chemokines are small chemotactic proteins that have a crucial role in leukocyte recruitment into tissue. Targeting these mediators has been suggested as a potential therapeutic option in inflammatory skin diseases such as psoriasis. Using quantitative RT-PCR, we found CCL7, a chemokine ligand known to interact with multiple C-C chemokine receptors, to be markedly increased in lesional psoriasis as opposed to atopic dermatitis, lichen planus, non-lesional psoriatic and normal control skin. Surprisingly, this increase in CCL7 mRNA expression exceeded that of all other chemokines investigated, and keratinocytes and dermal blood endothelial cells were identified as its likely cellular sources. In an imiquimod-induced psoriasis-like mouse model, CCL7 had a profound impact on myeloid cell inflammation as well as on the upregulation of key pro-psoriatic cytokines such as CCL20, IL-12p40 and IL-17C, while its blockade led to an increase in the antipsoriatic cytokine IL-4. In humans receiving the TNF-alpha-blocker infliximab, CCL7 was downregulated in lesional psoriatic skin already within 16 hours after a single intravenous infusion. These data suggest that CCL7 acts as a driver of TNF-alpha-dependent Th1/Th17-mediated inflammation in lesional psoriatic skin.
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Deligne, C., et al (2015). "Anti-CD20 therapy induces a memory Th1 response through the IFN-gamma/IL-12 axis and prevents protumor regulatory T-cell expansion in mice" Leukemia 29(4): 947-957.
PubMed
The long-lasting clinical response by lymphoma patients to anti-CD20 therapy has been attributed to the induction of an anti-tumor adaptive immunity. We previously demonstrated that a CD4-dependent mechanism is responsible for the long-term protection of CD20(+) tumor-bearing mice by anti-CD20 treatment. Here, we compare tumor immunity in tumor-bearing animals that did or did not receive anti-CD20 treatment. Splenic CD4(+)FoxP3(+) regulatory T cells (Tregs) expanded substantially in untreated mice that exhibited then a reduced survival, whereas Tregs depletion led to long-term survival of the animals, suggesting the establishment of a Treg-dependent immunosuppressive environment after tumor injection. Strikingly, anti-CD20 therapy reversed the initial expansion of Tregs, and was accompanied by a marked increase in the number of Th1 cells, with no detectable change in Th2 and Th17 cell numbers. Interleukin-12 serum level was also increased by the anti-CD20 treatment, and activated myeloid dendritic cells producing interleukin-12 could be detected in lymph nodes of treated animals, while interferon-gamma blockade strongly reduced survival. Also, CD4(+) effector memory T cells were evidenced in surviving animals, and the transfer of CD4(+) T cells induced long-term protection. Thus, anti-CD20 therapy promotes strong anti-tumor adaptive immunity, opposes Treg expansion and inhibits tumor cells from maintaining an immunosuppressive environment.
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Brunner, P. M., et al (2015). "CCL7 contributes to the TNF-alpha-dependent inflammation of lesional psoriatic skin" Exp Dermatol 24(7): 522-528.
PubMed
Chemokines are small chemotactic proteins that have a crucial role in leukocyte recruitment into tissue. Targeting these mediators has been suggested as a potential therapeutic option in inflammatory skin diseases such as psoriasis. Using quantitative RT-PCR, we found CCL7, a chemokine ligand known to interact with multiple C-C chemokine receptors, to be markedly increased in lesional psoriasis as opposed to atopic dermatitis, lichen planus, non-lesional psoriatic and normal control skin. Surprisingly, this increase in CCL7 mRNA expression exceeded that of all other chemokines investigated, and keratinocytes and dermal blood endothelial cells were identified as its likely cellular sources. In an imiquimod-induced psoriasis-like mouse model, CCL7 had a profound impact on myeloid cell inflammation as well as on the upregulation of key pro-psoriatic cytokines such as CCL20, IL-12p40 and IL-17C, while its blockade led to an increase in the antipsoriatic cytokine IL-4. In humans receiving the TNF-alpha-blocker infliximab, CCL7 was downregulated in lesional psoriatic skin already within 16 hours after a single intravenous infusion. These data suggest that CCL7 acts as a driver of TNF-alpha-dependent Th1/Th17-mediated inflammation in lesional psoriatic skin.
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Villegas-Mendez, A., et al (2015). "Parasite-specific CD4+IFN-gamma+IL-10+ T cells distribute within both lymphoid and non-lymphoid compartments and are controlled systemically by IL-27 and ICOS during blood-stage malaria infection" Infect Immun. pii
PubMed
Immune-mediated pathology in IL-10 deficient mice during blood-stage malaria infection typically manifests in non-lymphoid organs, such as the liver and lung. Thus, it is critical to define the cellular sources of IL-10 in these sensitive non-lymphoid compartments during infection. Moreover, it is important to determine if IL-10 production is controlled through conserved or disparate molecular programmes in distinct anatomical locations during malaria infection, as this may enable spatiotemporal tuning of the regulatory immune response. In this study, using dual IFN-gamma-YFP and IL-10-GFP reporter mice we show that CD4+YFP+ T cells are the major source of IL-10 in both lymphoid and non-lymphoid compartments throughout the course of blood-stage P. yoelii infection. Mature splenic CD4+YFP+GFP+ T cells, which preferentially expressed high levels of CCR5, were capable of migrating to and seeding the non-lymphoid tissues, indicating that the systemically distributed host-protective cells have a common developmental history. Despite exhibiting comparable phenotypes, CD4+YFP+GFP+ T cells from the liver and lung produced significantly higher quantities of IL-10 than their splenic counterparts, showing that the CD4+YFP+GFP+ T cells exert graded functions in distinct tissue locations during infection. Unexpectedly, given the unique environmental conditions within discrete non-lymphoid and lymphoid organs, we show that IL-10 production by CD4+YFP+ T cells is controlled systemically during malaria infection through IL-27R signalling that is supported post-CD4+ T cell priming by ICOS signalling. The results in this study substantially improve our understanding of the systemic IL-10 response to malaria infection, particularly within sensitive non-lymphoid organs.
Product Citations
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IL-12/IL-23 neutralization is ineffective for alopecia areata in mice and humans.
In The Journal of Allergy and Clinical Immunology on 1 December 2019 by Ortolan, L. S., Kim, S. R., et al.
PubMed
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Genetic inhibition of IL-12β suppresses systolic overload-induced cardiac oxidative stress, inflammation, and heart failure development.
In Redox Biol on 1 April 2026 by Bhattarai, U., Niu, Z., et al.
PubMed
Inflammation is a key factor in the development of heart failure (HF), with interleukin-12 (IL-12) and interleukin-23 (IL-23) acting as significant pro-inflammatory cytokines, both of which are simultaneously reduced by inhibiting IL-12β. This study utilized IL-12β knockout (KO) mice to investigate whether genetically inhibiting IL-12β could lessen transverse aortic constriction (TAC)-induced cardiac inflammation, hypertrophy, and dysfunction, as well as associated lung remodeling. We found that IL-12β KO significantly improved TAC-induced cardiac dysfunction in both male and female mice, evidenced by better left ventricular (LV) ejection fraction and fractional shortening. Additionally, IL-12β KO substantially reduced the TAC-induced increases in the weight of the LV, left atrium, lung, and right ventricle (RV), and their ratios to body weight or tibial length in both sexes. Furthermore, IL-12β KO markedly attenuated TAC-induced LV leukocyte infiltration, cardiomyocyte hypertrophy, fibrosis, and subsequent lung inflammation and remodeling. Bulk LV RNA sequencing demonstrated that IL-12β KO also mitigated TAC-induced changes in LV gene profiles linked to inflammation and fibrosis. We also found that IL-12β KO significantly reduced TAC-induced LV accumulation of various immune cell subsets, activation of CD4+ and CD8+ T cells, and the percentage of central memory CD4+ and CD8+ T cells within the cardiac drainage lymph nodes. Moreover, IL-12β KO mice exhibited a significant reduction in IFNγ+CD8+ and CXCR3+CD8+ T cells in the drainage lymph nodes compared to wild-type mice after TAC. Finally, IL-12β KO and IL-12β blocking antibody significantly decreased TAC-induced LV production of reactive oxygen species (ROS) and the expression of 3-nitrotyrosine (3-NT) and 4-hydroxynonenal (4-HNE). Collectively, these findings underscore the critical role of IL-12β in systolic overload-induced LV inflammation and HF, likely through mediating cardiac immune cell accumulation, oxidative stress, and fibrosis.
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Genetic inhibition of IL-12β suppresses systolic overload-induced cardiac oxidative stress, inflammation, and heart failure development.
In Redox Biol on 1 April 2026 by Bhattarai, U., Niu, Z., et al.
PubMed
Inflammation is a key factor in the development of heart failure (HF), with interleukin-12 (IL-12) and interleukin-23 (IL-23) acting as significant pro-inflammatory cytokines, both of which are simultaneously reduced by inhibiting IL-12β. This study utilized IL-12β knockout (KO) mice to investigate whether genetically inhibiting IL-12β could lessen transverse aortic constriction (TAC)-induced cardiac inflammation, hypertrophy, and dysfunction, as well as associated lung remodeling. We found that IL-12β KO significantly improved TAC-induced cardiac dysfunction in both male and female mice, evidenced by better left ventricular (LV) ejection fraction and fractional shortening. Additionally, IL-12β KO substantially reduced the TAC-induced increases in the weight of the LV, left atrium, lung, and right ventricle (RV), and their ratios to body weight or tibial length in both sexes. Furthermore, IL-12β KO markedly attenuated TAC-induced LV leukocyte infiltration, cardiomyocyte hypertrophy, fibrosis, and subsequent lung inflammation and remodeling. Bulk LV RNA sequencing demonstrated that IL-12β KO also mitigated TAC-induced changes in LV gene profiles linked to inflammation and fibrosis. We also found that IL-12β KO significantly reduced TAC-induced LV accumulation of various immune cell subsets, activation of CD4+ and CD8+ T cells, and the percentage of central memory CD4+ and CD8+ T cells within the cardiac drainage lymph nodes. Moreover, IL-12β KO mice exhibited a significant reduction in IFNγ+CD8+ and CXCR3+CD8+ T cells in the drainage lymph nodes compared to wild-type mice after TAC. Finally, IL-12β KO and IL-12β blocking antibody significantly decreased TAC-induced LV production of reactive oxygen species (ROS) and the expression of 3-nitrotyrosine (3-NT) and 4-hydroxynonenal (4-HNE). Collectively, these findings underscore the critical role of IL-12β in systolic overload-induced LV inflammation and HF, likely through mediating cardiac immune cell accumulation, oxidative stress, and fibrosis.
-
Genetic inhibition of IL-12β suppresses systolic overload-induced cardiac oxidative stress, inflammation, and heart failure development.
In Redox Biol on 1 April 2026 by Bhattarai, U., Niu, Z., et al.
PubMed
Inflammation is a key factor in the development of heart failure (HF), with interleukin-12 (IL-12) and interleukin-23 (IL-23) acting as significant pro-inflammatory cytokines, both of which are simultaneously reduced by inhibiting IL-12β. This study utilized IL-12β knockout (KO) mice to investigate whether genetically inhibiting IL-12β could lessen transverse aortic constriction (TAC)-induced cardiac inflammation, hypertrophy, and dysfunction, as well as associated lung remodeling. We found that IL-12β KO significantly improved TAC-induced cardiac dysfunction in both male and female mice, evidenced by better left ventricular (LV) ejection fraction and fractional shortening. Additionally, IL-12β KO substantially reduced the TAC-induced increases in the weight of the LV, left atrium, lung, and right ventricle (RV), and their ratios to body weight or tibial length in both sexes. Furthermore, IL-12β KO markedly attenuated TAC-induced LV leukocyte infiltration, cardiomyocyte hypertrophy, fibrosis, and subsequent lung inflammation and remodeling. Bulk LV RNA sequencing demonstrated that IL-12β KO also mitigated TAC-induced changes in LV gene profiles linked to inflammation and fibrosis. We also found that IL-12β KO significantly reduced TAC-induced LV accumulation of various immune cell subsets, activation of CD4+ and CD8+ T cells, and the percentage of central memory CD4+ and CD8+ T cells within the cardiac drainage lymph nodes. Moreover, IL-12β KO mice exhibited a significant reduction in IFNγ+CD8+ and CXCR3+CD8+ T cells in the drainage lymph nodes compared to wild-type mice after TAC. Finally, IL-12β KO and IL-12β blocking antibody significantly decreased TAC-induced LV production of reactive oxygen species (ROS) and the expression of 3-nitrotyrosine (3-NT) and 4-hydroxynonenal (4-HNE). Collectively, these findings underscore the critical role of IL-12β in systolic overload-induced LV inflammation and HF, likely through mediating cardiac immune cell accumulation, oxidative stress, and fibrosis.