InVivoMAb anti-mouse TNFα
Product Description
Specifications
| Isotype | Rat IgG1 |
|---|---|
| Recommended Isotype Control(s) | InVivoMAb rat IgG1 isotype control, anti-horseradish peroxidase |
| Recommended Dilution Buffer | InVivoPure pH 8.0 Dilution Buffer |
| Conjugation | This product is unconjugated. Conjugation is available via our Antibody Conjugation Services. |
| Immunogen | Recombinant mouse TNFα |
| Reported Applications |
in vivo TNFα neutralization in vitro TNFα neutralization Western blot |
| Formulation |
PBS, pH 8.0 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_1107764 |
| 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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Deng, L., et al (2014). "Irradiation and anti-PD-L1 treatment synergistically promote antitumor immunity in mice" J Clin Invest 124(2): 687-695.
PubMed
High-dose ionizing irradiation (IR) results in direct tumor cell death and augments tumor-specific immunity, which enhances tumor control both locally and distantly. Unfortunately, local relapses often occur following IR treatment, indicating that IR-induced responses are inadequate to maintain antitumor immunity. Therapeutic blockade of the T cell negative regulator programmed death-ligand 1 (PD-L1, also called B7-H1) can enhance T cell effector function when PD-L1 is expressed in chronically inflamed tissues and tumors. Here, we demonstrate that PD-L1 was upregulated in the tumor microenvironment after IR. Administration of anti-PD-L1 enhanced the efficacy of IR through a cytotoxic T cell-dependent mechanism. Concomitant with IR-mediated tumor regression, we observed that IR and anti-PD-L1 synergistically reduced the local accumulation of tumor-infiltrating myeloid-derived suppressor cells (MDSCs), which suppress T cells and alter the tumor immune microenvironment. Furthermore, activation of cytotoxic T cells with combination therapy mediated the reduction of MDSCs in tumors through the cytotoxic actions of TNF. Our data provide evidence for a close interaction between IR, T cells, and the PD-L1/PD-1 axis and establish a basis for the rational design of combination therapy with immune modulators and radiotherapy.
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Shaabani, N., et al (2018). "The probacterial effect of type I interferon signaling requires its own negative regulator USP18" Sci Immunol 3(27).
PubMed
Type I interferon (IFN-I) signaling paradoxically impairs host immune responses during many primary and secondary bacterial infections. Lack of IFN-I receptor reduces bacterial replication and/or bacterial persistence during infection with several bacteria. However, the mechanisms that mediate the adverse IFN-I effect are incompletely understood. Here, we show that Usp18, an interferon-stimulated gene that negatively regulates IFN-I signaling, is primarily responsible for the deleterious effect of IFN-I signaling during infection of mice with Listeria monocytogenes or Staphylococcus aureus Mechanistically, USP18 promoted bacterial replication by inhibiting antibacterial tumor necrosis factor-alpha (TNF-alpha) signaling. Deleting IFNAR1 or USP18 in CD11c-Cre(+) cells similarly reduced bacterial titers in multiple organs and enhanced survival. Our results demonstrate that inhibiting USP18 function can promote control of primary and secondary bacterial infection by enhancing the antibacterial effect of TNF-alpha, which correlates with induction of reactive oxygen species (ROS). These findings suggest that USP18 could be targeted therapeutically in patients to ameliorate disease caused by serious bacterial infections.
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Baeyens, A., et al (2015). "Effector T cells boost regulatory T cell expansion by IL-2, TNF, OX40, and plasmacytoid dendritic cells depending on the immune context" J Immunol 194(3): 999-1010.
PubMed
CD4(+)CD25(+)Foxp3(+) regulatory T (Treg) cells play a major role in peripheral tolerance. Multiple environmental factors and cell types affect their biology. Among them, activated effector CD4(+) T cells can boost Treg cell expansion through TNF or IL-2. In this study, we further characterized this effector T (Teff) cell-dependent Treg cell boost in vivo in mice. This phenomenon was observed when both Treg and Teff cells were activated by their cognate Ag, with the latter being the same or different. Also, when Treg cells highly proliferated on their own, there was no additional Treg cell boost by Teff cells. In a condition of low inflammation, the Teff cell-mediated Treg cell boost involved TNF, OX40L, and plasmacytoid dendritic cells, whereas in a condition of high inflammation, it involved TNF and IL-2. Thus, this feedback mechanism in which Treg cells are highly activated by their Teff cell counterparts depends on the immune context for its effectiveness and mechanism. This Teff cell-dependent Treg cell boost may be crucial to limit inflammatory and autoimmune responses.
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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.
Product Citations
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Lymphodepleting preconditioning impairs host antitumor immunity induced by adoptive T cell therapy in mouse models.
In Nat Commun on 31 March 2026 by Figueroa, D., Vega, J. P., et al.
PubMed
Adoptive T cell therapy (ACT) is effective against hematologic cancers, but the mechanisms underlying durable responses in solid tumors remain unclear. We show that adoptively transferred CD8+ T cells that eradicate established murine tumors promote expansion of host CD8+ T cells exhibiting tumor-reactive and tissue-resident phenotypes that contribute to tumor elimination. Mechanistically, tumor necrosis factor (TNF) from transferred cells induces dendritic cell (DC)-dependent expansion of host CD8+ T cells, conferring protection against ACT-resistant tumor cells lacking the targeted antigen. Lymphodepleting preconditioning promotes expansion of transferred cells and primary tumor eradication but impairs host antitumor immunity and abrogates protection against ACT-resistant tumors. In human tumors, increased TNF/DC/CD8+ T cell profiles correlate with favorable ACT responses and improved survival. These findings reveal a TNF-dependent interplay between transferred and host CD8+ T cells underlying durable antitumor immunity that is impaired by lymphodepleting preconditioning in mouse models, suggesting an underappreciated mechanism of ACT resistance.
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TNF-mediated hilar interneuron loss and aberrant granule cell migration are associated with chronic cognitive deficits following TBI.
In Brain Behav Immun on 1 March 2026 by Harris, E. A., Budianto, S., et al.
PubMed
Chronic morbidities, including cognitive impairment, are a common consequence of traumatic brain injury (TBI), with millions currently living with permanent TBI-related disabilities. Recent work has indicated that altered cellular architecture in the dentate gyrus (DG) may play a significant role in the development of chronic cognitive impairment and excitotoxicity. However, current understanding of the temporal progression of these pathological changes in the context of neuroinflammation and chronic cognitive outcomes is limited. This study characterized temporospatial changes in the hilar region of the DG, showing that the population of reelin- and somatostatin-expressing inhibitory interneurons was significantly reduced as early as 7 days post-injury (dpi), and that aberrant migration of excitatory granule cells occurs gradually in the weeks to months following injury. These findings coincided with upregulation of monocyte/macrophage-associated inflammatory mediators, including MIP-1β, MIG, MCP-1, and TNF-α at 7 days dpi, with differential cytokine regulation persisting 120 dpi. Injury was associated with the development of chronic spatial memory impairment and reduced risk-assessment behavior, with a transient reduction in spontaneous anxiety. TNFR1 and TNFR2 were differentially expressed in inhibitory neurons, further implicating TNF-signaling as a driver of hilar neuron loss. Furthermore, systemic administration of anti-TNF-α monoclonal antibody induced significant neuroprotection, attenuated pro-inflammatory mediators, and hilar interneuron loss. These findings suggest that TNF-TNFR signaling plays a crucial role in driving hilar interneuron loss and aberrant granule cell migration, which, in turn, may contribute to the development of excitotoxicity and chronic cognitive deficits.
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TNF-mediated hilar interneuron loss and aberrant granule cell migration are associated with chronic cognitive deficits following TBI.
In Brain Behav Immun on 1 March 2026 by Harris, E. A., Budianto, S., et al.
PubMed
Chronic morbidities, including cognitive impairment, are a common consequence of traumatic brain injury (TBI), with millions currently living with permanent TBI-related disabilities. Recent work has indicated that altered cellular architecture in the dentate gyrus (DG) may play a significant role in the development of chronic cognitive impairment and excitotoxicity. However, current understanding of the temporal progression of these pathological changes in the context of neuroinflammation and chronic cognitive outcomes is limited. This study characterized temporospatial changes in the hilar region of the DG, showing that the population of reelin- and somatostatin-expressing inhibitory interneurons was significantly reduced as early as 7 days post-injury (dpi), and that aberrant migration of excitatory granule cells occurs gradually in the weeks to months following injury. These findings coincided with upregulation of monocyte/macrophage-associated inflammatory mediators, including MIP-1β, MIG, MCP-1, and TNF-α at 7 days dpi, with differential cytokine regulation persisting 120 dpi. Injury was associated with the development of chronic spatial memory impairment and reduced risk-assessment behavior, with a transient reduction in spontaneous anxiety. TNFR1 and TNFR2 were differentially expressed in inhibitory neurons, further implicating TNF-signaling as a driver of hilar neuron loss. Furthermore, systemic administration of anti-TNF-α monoclonal antibody induced significant neuroprotection, attenuated pro-inflammatory mediators, and hilar interneuron loss. These findings suggest that TNF-TNFR signaling plays a crucial role in driving hilar interneuron loss and aberrant granule cell migration, which, in turn, may contribute to the development of excitotoxicity and chronic cognitive deficits.
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Engineered bacteria launch and control an oncolytic virus.
In Nat Biomed Eng on 1 March 2026 by Singer, Z. S., Pabon, J., et al.
PubMed
The ability of bacteria and viruses to selectively replicate in tumours has led to synthetic engineering of new microbial therapies. Here we design a cooperative strategy whereby Salmonella typhimurium bacteria transcribe and deliver the Senecavirus A RNA genome inside host cells, launching a potent oncolytic viral infection. 'Encapsidated' by bacteria, the viral genome can further bypass circulating antiviral antibodies to reach the tumour and initiate replication and spread within immune mice. Finally, we engineer the virus to require a bacterially delivered protease to achieve virion maturation, demonstrating bacterial control over the virus. Together, we refer to this platform as 'CAPPSID' for Coordinated Activity of Prokaryote and Picornavirus for Safe Intracellular Delivery. This work extends bacterially delivered therapeutics to viral genomes, and shows how a consortium of microbes can achieve a cooperative aim.