InVivoMAb anti-mouse IL-6
Product Description
Specifications
| Isotype | Rat IgG1, κ |
|---|---|
| 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 | Recombinant mouse IL-6 |
| Reported Applications |
in vivo IL-6 neutralization in vitro IL-6 neutralization |
| 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_1107709 |
| 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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Khmaladze, I., et al (2014). "Mannan induces ROS-regulated, IL-17A-dependent psoriasis arthritis-like disease in mice" Proc Natl Acad Sci U S A 111(35): E3669-3678.
PubMed
Psoriasis (Ps) and psoriasis arthritis (PsA) are poorly understood common diseases, induced by unknown environmental factors, affecting skin and articular joints. A single i.p. exposure to mannan from Saccharomyces cerevisiae induced an acute inflammation in inbred mouse strains resembling human Ps and PsA-like disease, whereas multiple injections induced a relapsing disease. Exacerbation of disease severity was observed in mice deficient for generation of reactive oxygen species (ROS). Interestingly, restoration of ROS production, specifically in macrophages, ameliorated both skin and joint disease. Neutralization of IL-17A, mainly produced by gammadelta T cells, completely blocked disease symptoms. Furthermore, mice depleted of granulocytes were resistant to disease development. In contrast, certain acute inflammatory mediators (C5, Fcgamma receptor III, mast cells, and histamine) and adaptive immune players (alphabeta T and B cells) were redundant in disease induction. Hence, we propose that mannan-induced activation of macrophages leads to TNF-alpha secretion and stimulation of local gammadelta T cells secreting IL-17A. The combined action of activated macrophages and IL-17A produced in situ drives neutrophil infiltration in the epidermis and dermis of the skin, leading to disease manifestations. Thus, our finding suggests a new mechanism triggered by exposure to exogenous microbial components, such as mannan, that can induce and exacerbate Ps and PsA.
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Berger, H., et al (2013). "SOCS3 transactivation by PPARgamma prevents IL-17-driven cancer growth" Cancer Res 73(12): 3578-3590.
PubMed
Activation of the transcription factor PPARgamma by the n-3 fatty acid docosahexaenoic acid (DHA) is implicated in controlling proinflammatory cytokine secretion, but the intracellular signaling pathways engaged by PPARgamma are incompletely characterized. Here, we identify the adapter-encoding gene SOCS3 as a critical transcriptional target of PPARgamma. SOCS3 promoter binding and gene transactivation by PPARgamma was associated with a repression in differentiation of proinflammatory T-helper (TH)17 cells. Accordingly, TH17 cells induced in vitro displayed increased SOCS3 expression and diminished capacity to produce interleukin (IL)-17 following activation of PPARgamma by DHA. Furthermore, naive CD4 T cells derived from mice fed a DHA-enriched diet displayed less capability to differentiate into TH17 cells. In two different mouse models of cancer, DHA prevented tumor outgrowth and angiogenesis in an IL-17-dependent manner. Altogether, our results uncover a novel molecular pathway by which PPARgamma-induced SOCS3 expression prevents IL-17-mediated cancer growth.
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Benevides, L., et al (2015). "IL17 Promotes Mammary Tumor Progression by Changing the Behavior of Tumor Cells and Eliciting Tumorigenic Neutrophils Recruitment" Cancer Res 75(18): 3788-3799.
PubMed
The aggressiveness of invasive ductal carcinoma (IDC) of the breast is associated with increased IL17 levels. Studying the role of IL17 in invasive breast tumor pathogenesis, we found that metastatic primary tumor-infiltrating T lymphocytes produced elevated levels of IL17, whereas IL17 neutralization inhibited tumor growth and prevented the migration of neutrophils and tumor cells to secondary disease sites. Tumorigenic neutrophils promote disease progression, producing CXCL1, MMP9, VEGF, and TNFalpha, and their depletion suppressed tumor growth. IL17A also induced IL6 and CCL20 production in metastatic tumor cells, favoring the recruitment and differentiation of Th17. In addition, IL17A changed the gene-expression profile and the behavior of nonmetastatic tumor cells, causing tumor growth in vivo, confirming the protumor role of IL17. Furthermore, high IL17 expression was associated with lower disease-free survival and worse prognosis in IDC patients. Thus, IL17 blockade represents an attractive approach for the control of invasive breast tumors. Cancer Res; 75(18); 3788-99. (c)2015 AACR.
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Kugler, D. G., et al (2013). "CD4+ T cells are trigger and target of the glucocorticoid response that prevents lethal immunopathology in toxoplasma infection" J Exp Med 210(10): 1919-1927.
PubMed
Synthetic glucocorticoids (GCs) are commonly used in the treatment of inflammatory diseases, but the role of endogenous GCs in the regulation of host-protective immune responses is poorly understood. Here we show that GCs are induced during acute Toxoplasma gondii infection and directly control the T cell response to the parasite. When infected with toxoplasma, mice that selectively lack GC receptor (GR) expression in T cells (GR(lck-Cre)) rapidly succumb to infection despite displaying parasite burdens indistinguishable from control animals and unaltered levels of the innate cytokines IL-12 and IL-27. Mortality in the GR(lck-Cre) mice was associated with immunopathology and hyperactive Th1 cell function as revealed by enhanced IFN-gamma and TNF production in vivo. Unexpectedly, these CD4(+) T lymphocytes also overexpressed IL-10. Importantly, CD4(+) T cell depletion in wild-type or GR(lck-Cre) mice led to ablation of the GC response to infection. Moreover, in toxoplasma-infected RAG(-/-) animals, adoptive transfer of CD4(+) T lymphocytes was required for GC induction. These findings establish a novel IL-10-independent immunomodulatory circuit in which CD4(+) T cells trigger a GC response that in turn dampens their own effector function. In the case of T. gondii infection, this self-regulatory pathway is critical for preventing collateral tissue damage and promoting host survival.
Product Citations
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Tumoral extracellular vesicles and particles reprogram interstitial macrophages in the lung to promote vascular permeability and metastasis.
In Nat Cancer on 1 August 2026 by Dror, S., Wortzel, I., et al.
PubMed
The mechanisms by which tumor-derived extracellular vesicles and particles (EVPs) promote vascular permeability during premetastatic niche formation remain unclear. Here, we show that tumor EVPs rapidly induce vascular leakiness within 1 h of administration in female mice, creating a permissive environment that enhances metastatic seeding. Rather than acting directly on endothelial cells, EVPs activate NF-κB and JAK-STAT signaling in interstitial macrophages, leading to IL-6 secretion and increased vascular permeability. Interstitial macrophage depletion markedly reduces EVP-induced vascular leakiness and metastasis. We identify extracellular vesicle-associated integrin α5 (ITGα5) as a major functional determinant of this process, promoting macrophage activation and IL-6 secretion without affecting EVP uptake. EVPs derived from colorectal cancer tumors with high ITGα5 similarly induce macrophage IL-6 secretion and vascular permeability. Together, these findings define an EVP-macrophage-IL-6 axis that drives vascular permeability during premetastatic niche formation and identify EVP-associated ITGα5 as a key mediator of metastatic progression and a potential therapeutic target.
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Lysosome self-sorting nanodegraders for hepatic clearance of pathogenic serum mediators.
In Nat Nanotechnol on 1 August 2026 by Wu, J., Liu, X., et al.
PubMed
Extracellular targeted protein degradation is an emerging therapeutic strategy but has been rarely explored for clearing circulating pathogenic mediators. Here we report stiffness-oriented lysosome self-sorting nanodegraders (SOLIDs) for hepatic lysosomal degradation of serum immune mediators. SOLIDs feature a rigid semiconducting polymer core that is revealed for the first time to confer near-quantitative lysosomal accumulation across diverse cell types. After surface bioconjugation, SOLIDs capture the immune mediators of interest from blood via controlled protein corona formation. The resulting corona composition directs biodistribution, producing predominant accumulation in the liver, where they get degraded in hepatic lysosomes. We show that IL-6-capturing SOLIDs reduced serum IL-6 by an additional 70% versus IL-6 antibody therapy and increased 7-day survival in a murine sepsis model from 0% to 66.7%. In an acute lung injury model, CpG-capturing SOLIDs reduced pulmonary immune cell infiltration 1.7-fold relative to CpG neutralization and suppressed expression of co-stimulatory molecules. This work identifies nanoparticle mechanics as a critical factor in organelle targeting and proposes a nano-therapeutic approach for the degradation of pathogenic serum biomolecules.
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IL6 Supports Development of an Immunosuppressive Microenvironment and Resistance to Therapy in Glioblastoma.
In Cancer Res on 15 July 2026 by Young, J. S., Cho, N. W., et al.
PubMed
The glioblastoma tumor-immune microenvironment (TIME) is an immunosuppressive barrier to therapy that encumbers glioblastoma responses to immune checkpoint inhibition (ICI). Immunosuppressive cytokines, protumor macrophages and myeloid cells, and exhausted T cells are all hallmarks of the glioblastoma TIME. In this study, we integrated spatial and single-cell analyses of patient-matched human glioblastoma samples before and after ICI treatment with genetic, immunologic, single-cell, and pharmacologic studies in preclinical models to show that interleukin 6 (IL6) neutralization reprograms the glioblastoma TIME to sensitize mouse glioblastoma allografts to ICI and radiotherapy. Rare human glioblastomas that achieved clinical responses to ICI had lower pretreatment IL6 levels compared with glioblastomas that did not respond to ICI. Diverse immunostimulatory gene therapies suppressed local IL6 levels in mouse glioblastoma allografts, and IL6 from glioblastoma cells and the tumor microenvironment was associated with reduced survival in preclinical models and in patients. IL6 blockade with a neutralizing antibody transiently sensitized mouse glioblastoma allografts to ICI by decreasing immunosuppressive regulatory T cells and increasing MHCII+ monocytes, CD103+ migratory dendritic cells (DC), CD11b+ conventional DCs, and effector CD8+ T cells. IL6 blockade plus ICI sensitized mouse glioblastoma allografts to immunostimulatory ablative radiotherapy. Together, these data suggest that IL6 signaling contributes to ICI resistance in glioblastoma and provides a combination treatment strategy that could be used for patients.
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IL6 Supports Development of an Immunosuppressive Microenvironment and Resistance to Therapy in Glioblastoma.
In Cancer Res on 15 July 2026 by Young, J. S., Cho, N. W., et al.
PubMed
The glioblastoma tumor-immune microenvironment (TIME) is an immunosuppressive barrier to therapy that encumbers glioblastoma responses to immune checkpoint inhibition (ICI). Immunosuppressive cytokines, protumor macrophages and myeloid cells, and exhausted T cells are all hallmarks of the glioblastoma TIME. In this study, we integrated spatial and single-cell analyses of patient-matched human glioblastoma samples before and after ICI treatment with genetic, immunologic, single-cell, and pharmacologic studies in preclinical models to show that interleukin 6 (IL6) neutralization reprograms the glioblastoma TIME to sensitize mouse glioblastoma allografts to ICI and radiotherapy. Rare human glioblastomas that achieved clinical responses to ICI had lower pretreatment IL6 levels compared with glioblastomas that did not respond to ICI. Diverse immunostimulatory gene therapies suppressed local IL6 levels in mouse glioblastoma allografts, and IL6 from glioblastoma cells and the tumor microenvironment was associated with reduced survival in preclinical models and in patients. IL6 blockade with a neutralizing antibody transiently sensitized mouse glioblastoma allografts to ICI by decreasing immunosuppressive regulatory T cells and increasing MHCII+ monocytes, CD103+ migratory dendritic cells (DC), CD11b+ conventional DCs, and effector CD8+ T cells. IL6 blockade plus ICI sensitized mouse glioblastoma allografts to immunostimulatory ablative radiotherapy. Together, these data suggest that IL6 signaling contributes to ICI resistance in glioblastoma and provides a combination treatment strategy that could be used for patients.