InVivoMAb mouse IgG1 isotype control, unknown specificity
Product Description
Specifications
| Isotype | Mouse IgG1, κ |
|---|---|
| Recommended Dilution Buffer | InVivoPure pH 6.5 Dilution Buffer |
| Conjugation | This product is unconjugated. Conjugation is available via our Antibody Conjugation Services. |
| Formulation |
PBS, pH 6.5 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_1107784 |
| 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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Leon, B., et al (2014). "FoxP3+ regulatory T cells promote influenza-specific Tfh responses by controlling IL-2 availability" Nat Commun 5: 3495.
PubMed
Here, we test the role of FoxP3(+) regulatory T cells (Tregs) in controlling T follicular helper (Tfh) and germinal centre (GC) B-cell responses to influenza. In contrast to the idea that Tregs suppress T-cell responses, we find that Treg depletion severely reduces the Tfh cell response to influenza virus. Furthermore, Treg depletion prevents the accumulation of influenza-specific GCs. These effects are not due to alterations in TGFbeta availability or a precursor-progeny relationship between Tregs and Tfh cells, but are instead mediated by increased availability of IL-2, which suppresses the differentiation of Tfh cells and as a consequence, compromises the GC B response. Thus, Tregs promote influenza-specific GC responses by preventing excessive IL-2 signalling, which suppresses Tfh cell differentiation.
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Faraco, G., et al (2018). "Dietary salt promotes neurovascular and cognitive dysfunction through a gut-initiated TH17 response" Nat Neurosci 21(2): 240-249.
PubMed
A diet rich in salt is linked to an increased risk of cerebrovascular diseases and dementia, but it remains unclear how dietary salt harms the brain. We report that, in mice, excess dietary salt suppresses resting cerebral blood flow and endothelial function, leading to cognitive impairment. The effect depends on expansion of TH17 cells in the small intestine, resulting in a marked increase in plasma interleukin-17 (IL-17). Circulating IL-17, in turn, promotes endothelial dysfunction and cognitive impairment by the Rho kinase-dependent inhibitory phosphorylation of endothelial nitric oxide synthase and reduced nitric oxide production in cerebral endothelial cells. The findings reveal a new gut-brain axis linking dietary habits to cognitive impairment through a gut-initiated adaptive immune response compromising brain function via circulating IL-17. Thus, the TH17 cell-IL-17 pathway is a putative target to counter the deleterious brain effects induced by dietary salt and other diseases associated with TH17 polarization.
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Sell, S., et al (2015). "Control of murine cytomegalovirus infection by gammadelta T cells" PLoS Pathog 11(2): e1004481.
PubMed
Infections with cytomegalovirus (CMV) can cause severe disease in immunosuppressed patients and infected newborns. Innate as well as cellular and humoral adaptive immune effector functions contribute to the control of CMV in immunocompetent individuals. None of the innate or adaptive immune functions are essential for virus control, however. Expansion of gammadelta T cells has been observed during human CMV (HCMV) infection in the fetus and in transplant patients with HCMV reactivation but the protective function of gammadelta T cells under these conditions remains unclear. Here we show for murine CMV (MCMV) infections that mice that lack CD8 and CD4 alphabeta-T cells as well as B lymphocytes can control a MCMV infection that is lethal in RAG-1(-/-) mice lacking any T- and B-cells. gammadelta T cells, isolated from infected mice can kill MCMV infected target cells in vitro and, importantly, provide long-term protection in infected RAG-1(-/-) mice after adoptive transfer. gammadelta T cells in MCMV infected hosts undergo a prominent and long-lasting phenotypic change most compatible with the view that the majority of the gammadelta T cell population persists in an effector/memory state even after resolution of the acute phase of the infection. A clonotypically focused Vgamma1 and Vgamma2 repertoire was observed at later stages of the infection in the organs where MCMV persists. These findings add gammadelta T cells as yet another protective component to the anti-CMV immune response. Our data provide clear evidence that gammadelta T cells can provide an effective control mechanism of acute CMV infections, particularly when conventional adaptive immune mechanisms are insufficient or absent, like in transplant patient or in the developing immune system in utero. The findings have implications in the stem cell transplant setting, as antigen recognition by gammadelta T cells is not MHC-restricted and dual reactivity against CMV and tumors has been described.
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Beug, S. T., et al (2014). "Smac mimetics and innate immune stimuli synergize to promote tumor death" Nat Biotechnol 32(2): 182-190.
PubMed
Smac mimetic compounds (SMC), a class of drugs that sensitize cells to apoptosis by counteracting the activity of inhibitor of apoptosis (IAP) proteins, have proven safe in phase 1 clinical trials in cancer patients. However, because SMCs act by enabling transduction of pro-apoptotic signals, SMC monotherapy may be efficacious only in the subset of patients whose tumors produce large quantities of death-inducing proteins such as inflammatory cytokines. Therefore, we reasoned that SMCs would synergize with agents that stimulate a potent yet safe “cytokine storm.” Here we show that oncolytic viruses and adjuvants such as poly(I:C) and CpG induce bystander death of cancer cells treated with SMCs that is mediated by interferon beta (IFN-beta), tumor necrosis factor alpha (TNF-alpha) and/or TNF-related apoptosis-inducing ligand (TRAIL). This combinatorial treatment resulted in tumor regression and extended survival in two mouse models of cancer. As these and other adjuvants have been proven safe in clinical trials, it may be worthwhile to explore their clinical efficacy in combination with SMCs.
Product Citations
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Long pentraxin 3 (PTX3) regulates IL-17A-mediated immunity to Leishmania major infection in mice.
In Front Immunol on 26 February 2026 by Gupta, G., Mou, Z., et al.
PubMed
Cutaneous leishmaniasis, caused by protozoan parasites of the Leishmania genus, remains a significant health concern in endemic regions such as the Middle-East, Asia, Latin America, and North Africa. The disease affects millions of people worldwide, with over one million new infections reported annually. Despite its health impact, there is currently no approved vaccine largely due to limited understanding of immunological mechanisms underlying protective immunity and disease pathogenesis. We previously reported that long pentraxin 3 (PTX3), a pattern recognition molecule involved in inflammation, tissue repair, and wound healing, is a negative regulator of immunity in primary Leishmania major infection. Specifically, we showed that PTX3 exacerbates disease by suppressing protective Th17 responses. Here, we extend these findings by showing that PTX3 also influences secondary (memory) immunity to L. major. PTX3-deficient (PTX3-/-) mice which had resolved a primary infection exhibited enhanced resistance to secondary challenge compared to their wild-type (WT) controls. This enhanced resistance correlated with higher frequencies of effector memory CD4+ T cells in the spleens and draining lymph nodes. Upon re-infection, healed PTX3-/- mice produced significantly more IL-17A, while levels of IFN-γ, TNF-α, and IL-10 were similar. In vivo BrdU incorporation assays further revealed increased proliferation of IL-17+ CD4+ T cells in PTX3-/- mice. Importantly, neutralization of IL-17A during secondary challenge abolished the enhanced resistance observed in PTX3-/- mice, confirming a central role of IL-17 in PTX3-regulated secondary immunity. Collectively, our findings identify PTX3 as a key regulator of secondary immunity in cutaneous leishmaniasis and underscores the importance of IL-17 in this process.
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A conserved eIF1A+ luminal cell-centered hypoxic and "cold" tumor microenvironment promotes pan-subtype prostate cancer progression.
In Cell Rep Med on 17 February 2026 by Cheng, Y., Wan, L., et al.
PubMed
Prostate cancer (PCa) is a malignancy with high heterogeneity arising from tumor microenvironment and histological subtypes. Identifying conserved progression drivers within such heterogeneity is essential for improving clinical outcomes. Using imaging mass cytometry, this study analyzes 38 proteins across paracancerous tissue and four histological subtypes: low-grade prostate acinar adenocarcinoma (LgPAC), high-grade PAC (HgPAC), intraductal carcinoma (IDC), and ductal adenocarcinoma (DAC). Results reveal that eIF1A is overexpressed in high-risk subtypes including HgPAC, IDC, and DAC and correlates with poor prognosis. In luminal cells, EIF1A knockdown and the translation inhibitor homoharringtonine (HHT) both suppress HIF-1α translation and tumor growth, while promoting infiltration of anticancer immune cells including PD-1- T cells and CD163- macrophages. Clinically, neoadjuvant HHT combined with androgen deprivation therapy reduces hypoxia and enhances immune cell infiltration, as shown by single-cell RNA sequencing. Collectively, this work defines conserved molecular features across PCa subtypes, providing promising insights for clinical management. This study was registered at Clinicaltrials.gov (NCT06834321).
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Ly6G+ granulocytes-derived IL-17 limits protective host responses and promotes tuberculosis pathogenesis.
In Elife on 5 February 2026 by Sharma, P., Sharma, R. D., et al.
PubMed
The protective correlates of Mycobacterium tuberculosis (Mtb) infection-elicited host immune responses are incompletely understood. Here, we report pro-pathogenic crosstalk involving Ly6G+ granulocytes (Ly6G+Gra), IL-17, and COX2. We show that in the lungs of Mtb-infected wild-type mice, either BCG-vaccinated or not, most intracellular bacilli are Ly6G+Gra-resident 4 weeks post-infection onwards. In the genetically susceptible ifng-/- mice, excessive Ly6G+Gra infiltration correlates with severe bacteremia. Neutralizing IL-17 (anti-IL17mAb) and COX2 inhibition by celecoxib reverse Ly6G+Gra infiltration, associated pathology, and death in ifng-/- mice. Surprisingly, Ly6G+Gra also serves as the major source of IL-17 in the lungs of Mtb-infected WT or ifng-/- mice. The IL-17-COX2-Ly6G+Gra interplay also operates in WT mice. Inhibiting RORγt, the key transcription factor for IL-17 production or COX2, reduces the bacterial burden in Ly6G+Gra, leading to reduced bacterial burden and pathology in the lungs of WT mice. In the Mtb-infected WT mice, COX2 inhibition abrogates IL-17 levels in the lung homogenates and significantly enhances BCG's protective efficacy, mainly by targeting the Ly6G+Gra-resident Mtb pool, a phenotype also observed when IL-17 is blocked by RORγt inhibitor. Furthermore, in pulmonary TB patients, high neutrophil count and IL-17 correlated with adverse treatment outcomes. Together, our results suggest that IL-17 and PGE2 are the negative correlates of protection, and we propose targeting the pro-pathogenic IL-17-COX2-Ly6G+Gra axis for TB prevention and therapy.
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Lymphotropic Virotherapy Induces DC and High Endothelial Venule Inflammation, Promoting the Antitumor Efficacy of Intratumor Virus Administration.
In Cancer Immunol Res on 3 February 2026 by Ludwig, A. L., McKay, Z. P., et al.
PubMed
Tumor-draining lymph nodes are a pivotal site for antitumor T-cell priming. However, their mechanistic roles in cancer immune surveillance and immunotherapy response remain poorly defined. Intratumor (IT) virotherapy generates antitumor T-cell immunity through multifaceted engagement of innate antiviral inflammation. In this study, we identify type-I interferon (IFNI) signaling in glioma-draining cervical lymph nodes as a mediator of IT polio virotherapy. Transient IFNI signaling after IT administration was rescued by cervical perilymphatic infusion (CPLI) virotherapy, targeting cervical lymph nodes directly. Dual-site (IT plus CPLI) virotherapy induced profound inflammatory reprogramming of cervical lymph nodes, enhanced viral RNA replication and IFNI signaling in dendritic cells and high endothelial venules, augmented antiglioma efficacy in mice, and was associated with T-cell activation in patients with recurrent glioblastoma. A phase II clinical trial of IT plus CPLI polio virotherapy is ongoing (NCT06177964). This study implicates the lymphatic system as a virotherapy target and demonstrates that CPLI virotherapy has the potential to complement brain tumor immunotherapy. See related Spotlight by Kaufman, p. 182.