InVivoMAb anti-mouse/rat IL-1β
Product Description
Specifications
| Isotype | Armenian Hamster IgG1 |
|---|---|
| Recommended Isotype Control(s) | InVivoMAb Armenian hamster IgG isotype control, anti-S. japonicum glutathione S-transferase |
| 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-1β |
| Reported Applications |
in vivo IL-1β neutralization in vitro IL-1β neutralization ELISA |
| 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_2687727 |
| 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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Coffelt, S. B., et al (2015). "IL-17-producing gammadelta T cells and neutrophils conspire to promote breast cancer metastasis" Nature 522(7556): 345-348.
PubMed
Metastatic disease remains the primary cause of death for patients with breast cancer. The different steps of the metastatic cascade rely on reciprocal interactions between cancer cells and their microenvironment. Within this local microenvironment and in distant organs, immune cells and their mediators are known to facilitate metastasis formation. However, the precise contribution of tumour-induced systemic inflammation to metastasis and the mechanisms regulating systemic inflammation are poorly understood. Here we show that tumours maximize their chance of metastasizing by evoking a systemic inflammatory cascade in mouse models of spontaneous breast cancer metastasis. We mechanistically demonstrate that interleukin (IL)-1beta elicits IL-17 expression from gamma delta (gammadelta) T cells, resulting in systemic, granulocyte colony-stimulating factor (G-CSF)-dependent expansion and polarization of neutrophils in mice bearing mammary tumours. Tumour-induced neutrophils acquire the ability to suppress cytotoxic T lymphocytes carrying the CD8 antigen, which limit the establishment of metastases. Neutralization of IL-17 or G-CSF and absence of gammadelta T cells prevents neutrophil accumulation and downregulates the T-cell-suppressive phenotype of neutrophils. Moreover, the absence of gammadelta T cells or neutrophils profoundly reduces pulmonary and lymph node metastases without influencing primary tumour progression. Our data indicate that targeting this novel cancer-cell-initiated domino effect within the immune system–the gammadelta T cell/IL-17/neutrophil axis–represents a new strategy to inhibit metastatic disease.
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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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Chen, K. W., et al (2014). "The neutrophil NLRC4 inflammasome selectively promotes IL-1beta maturation without pyroptosis during acute Salmonella challenge" Cell Rep 8(2): 570-582.
PubMed
The macrophage NLRC4 inflammasome drives potent innate immune responses against Salmonella by eliciting caspase-1-dependent proinflammatory cytokine production (e.g., interleukin-1beta [IL-1beta]) and pyroptotic cell death. However, the potential contribution of other cell types to inflammasome-mediated host defense against Salmonella was unclear. Here, we demonstrate that neutrophils, typically viewed as cellular targets of IL-1beta, themselves activate the NLRC4 inflammasome during acute Salmonella infection and are a major cell compartment for IL-1beta production during acute peritoneal challenge in vivo. Importantly, unlike macrophages, neutrophils do not undergo pyroptosis upon NLRC4 inflammasome activation. The resistance of neutrophils to pyroptotic death is unique among inflammasome-signaling cells so far described and allows neutrophils to sustain IL-1beta production at a site of infection without compromising the crucial inflammasome-independent antimicrobial effector functions that would be lost if neutrophils rapidly lysed upon caspase-1 activation. Inflammasome pathway modification in neutrophils thus maximizes host proinflammatory and antimicrobial responses during pathogen challenge.
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Gopinath, S., et al (2014). "Role of disease-associated tolerance in infectious superspreaders" Proc Natl Acad Sci U S A 111(44): 15780-15785.
PubMed
Natural populations show striking heterogeneity in their ability to transmit disease. For example, a minority of infected individuals known as superspreaders carries out the majority of pathogen transmission events. In a mouse model of Salmonella infection, a subset of infected hosts becomes superspreaders, shedding high levels of bacteria (>10(8) cfu per g of feces) but remain asymptomatic with a dampened systemic immune state. Here we show that superspreader hosts remain asymptomatic when they are treated with oral antibiotics. In contrast, nonsuperspreader Salmonella-infected hosts that are treated with oral antibiotics rapidly shed superspreader levels of the pathogen but display signs of morbidity. This morbidity is linked to an increase in inflammatory myeloid cells in the spleen followed by increased production of acute-phase proteins and proinflammatory cytokines. The degree of colonic inflammation is similar in antibiotic-treated superspreader and nonsuperspreader hosts, indicating that the superspreader hosts are tolerant of antibiotic-mediated perturbations in the intestinal tract. Importantly, neutralization of acute-phase proinflammatory cytokines in antibiotic-induced superspreaders suppresses the expansion of inflammatory myeloid cells and reduces morbidity. We describe a unique disease-associated tolerance to oral antibiotics in superspreaders that facilitates continued transmission of the pathogen.
Product Citations
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Microglial NLRP3-dependent pyroptosis promotes cognitive dysfunction of diabetic encephalopathy by inhibiting adult hippocampal neurogenesis through the release of IL-1β.
In Acta Pharmacol Sin on 1 August 2026 by Hua, M. Y., Huang, S., et al.
PubMed
Diabetic encephalopathy (DE) is a prevalent complication of diabetes which can lead to cognitive dysfunction, without effective therapy currently. In diabetic patients, a reduction in adult hippocampal neurogenesis (AHN) is a heightened risk of cognitive impairment, which may be associated with neuroinflammation caused by microglia. In this study, we established a DE mouse model and conducted in vitro cultures of microglial cells and neural stem cells. Our study demonstrated that the high-glucose associated with DE impairs AHN and induces microglial NOD-, LRR-, and pyrin domain-containing protein 3 (NLRP3) dependent pyroptosis. Further investigation showed that upregulation of microglial NLRP3 promotes the activation of Gasdermin D (GSDMD), the key pyroptosis effector, and the cleavage of pro-interleukin-1β (pro-IL-1β) by caspase-1, exacerbated pyroptosis and induced release of IL-1β, which might lead to impaired AHN and subsequent cognitive dysfunction. Conversely, downregulation of microglial NLRP3 inhibited caspase-1 activation and pyroptosis, reduced release of IL-1β, improved AHN, and rescued cognitive deficits in DE mouse model. Such findings suggest that targeting microglial NLRP3 inflammasome-mediated pyroptosis may be an important potential therapeutic target for treating DE.
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Trained immunity links hematopoietic stem cell aging to aging-associated inflammation.
In Nat Aging on 16 July 2026 by Mu, W. C., Barthez, M., et al.
PubMed
Trained immunity is a state of heightened immune response that is initiated in hematopoietic stem cells (HSCs) and mediated mainly by their myeloid progeny. Aging-associated inflammation drives many aging-related diseases, yet its biological origin is largely unknown. Here we show that SIRT3, a mitochondrial deacetylase highly expressed in HSCs but reduced during aging, suppresses the HSC response to aging that drives maladaptive trained immunity, chronic inflammation and tissue functional decline in mice. Overexpression of SIRT3 in HSCs not only ameliorates aging-associated HSC decline, but also improves the function of distant tissues, including attenuation of age-related declines in cognition and motility, via myeloid cells with modulated inflammatory programs. These findings reveal that HSC aging is a driver of aging-associated inflammation through maladaptive trained immunity and broaden the possible clinical applications of targeting HSCs from hematological diseases to include countering aging-associated physiological decline and improving healthspan.
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Mutation-dependent responses to sleep and exercise in clonal haematopoiesis.
In Nature on 1 July 2026 by Gerhardt, T., Jacob, W., et al.
PubMed
Clonal haematopoiesis (CH) activates inflammation and increases the risk of atherosclerosis1,2. Whether lifestyle alters CH clone expansion or the phenotypic programming of CH mutant cells, thereby affecting atherosclerosis, is unknown. Here, in humans and mice and across mutations in Jak2, Tet2, Trp53 and Dnmt3a, we demonstrate mutation-dependent responses to sleep and exercise in CH and show that mutant cells are uniquely sensitive to lifestyle. In two human datasets, moderate-to-vigorous physical activity was associated with lower prevalence of non-DNMT3A-driven CH. In atherogenic mice with Jak2V617F or Tet2 loss of function (LOF), but not Trp53 LOF or Dnmt3aR878H CH, uninterrupted sleep or exercise curtails clone expansion. In CH with the Jak2V617F mutation, sleep and exercise reduces clone expansion by selectively reprogramming mutant, but not cohabitant wild type, haematopoietic progenitor cells towards antiproliferative and metabolically healthy phenotypes by tempering bone marrow macrophage-haematopoietic progenitor cell IL-1β signalling. Sleep or exercise also lessens Jak2V617F-driven, Tet2 LOF-driven and Trp53 LOF-driven, but not Dnmt3aR878H-driven, atherosclerosis by locally reprogramming mutant vascular macrophages, independent of peripheral clone dynamics. In Jak2V617F, but not adjacent wild type, aortic macrophages, uninterrupted sleep blunts CLEC4E-dependent inflammasome activation, consequently diminishing lesions. Exercise, meanwhile, activates PAC1+ neurons in the locus coeruleus, raising the levels of peripheral noradrenaline, which signals through adrenergic receptor β2 (ADRβ2) whose expression is preserved by exercise in Jak2V617F, but not cohabitant wild type, aortic macrophages, selectively repressing their inflammatory programming and atherosclerosis. Our findings establish that healthy lifestyles gene-specifically diminish CH and selectively reprogram mutant haematopoietic progenitor cells and macrophages to maintain cardiovascular health.
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Inflammation-driven mitochondrial dysfunction and ROS accumulation orchestrate pulmonary fibrotic remodeling in sepsis.
In Redox Biol on 1 July 2026 by Zhong, Z., Wu, K., et al.
PubMed
Inflammation-induced pulmonary fibrosis is an irreversible and severe complication that leads to persistent decline in lung function and increased mortality; however, its early pathogenesis is still unclear. This study aimed to systematically elucidate the initiation mechanism of pulmonary fibrosis in the early stages of inflammation. By integrating multi-omics data and animal models, we found that lung exhibits stronger immune amplification and more severe mitochondrial dysfunction in comparison with other organs during inflammation, consequently fibrotic signaling is initiated in the acute phase. Mitochondria-related gene analysis identified six key genes (Bcl2l1, Gsr, Msrb3, AA467197, Stom, and Sod2) involved in the regulation of reactive oxygen species (ROS) metabolism, which were closely associated with clinical outcomes in sepsis. Temporal data and TNF-α/IL-1β intervention experiments revealed that these cytokines are persistently overexpressed in septic lungs, serving as critical drivers of ROS activation. In vitro assays further confirmed that ROS overload directly induces cellular damage and functional reprogramming of fibroblasts. Through bulk and single-cell transcriptomic analyses, we elucidated the alteration of intercellular communication between immune and parenchymal cells, and identified Col13a1+ fibroblasts as a key subpopulation with the capability to drive fibrotic remodeling. In conclusion, sustained TNF-α/IL-1β signaling in septic lungs exacerbates ROS accumulation, thereby driving aberrant fibroblast repair and initiating pulmonary fibrosis, in which Col13a1+ fibroblasts represent the major profibrotic subpopulation. Thus, the early inhibition of TNF-α/IL-1β expression, suppression of ROS accumulation, and regulation of Col13a1+ fibroblast activation may provide an effective therapeutic strategy for sepsis.