InVivoMAb anti-mouse IFNγ
in vitro IFNγ neutralization
ELISPOT
Flow cytometry
Western blotin vitro Organoids/Organ-on-Chip
Product Description
Bio X Cell is pleased to offer XMG1.2-CP058. XMG1.2-CP058 is a recombinant, chimeric version of the original XMG1.2 with identical variable domain sequences and constant region sequences converted from Rat IgG1, κ to mouse IgG1, κ for use in murine models. Species-matched chimeric antibodies exhibit regulated effector functions—including Fc receptor binding and complement activation—and cause less immunogenicity and formation of anti-drug antibodies (ADAs) than xenogenic antibodies in animal models. The highly controlled sequence and lack of genetic drift in recombinant antibodies provide more reliable and reproducible results over hybridoma derived antibodies.
Specifications
| Isotype | Rat IgG1, κ |
|---|---|
| Recommended Isotype Control(s) | InVivoMAb rat IgG1 isotype control, anti-horseradish peroxidase |
| Recommended Dilution Buffer | InVivoPure pH 8.0T Dilution Buffer |
| Conjugation | This product is unconjugated. Conjugation is available via our Antibody Conjugation Services. |
| Immunogen | Recombinant mouse IFNγ |
| Reported Applications |
in vivo IFNγ neutralization in vitro IFNγ neutralization ELISPOT Flow cytometry Western blotin vitro Organoids/Organ-on-Chip |
| Formulation |
PBS + 0.01% Tween, 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_1107694 |
| 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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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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Uddin, M. N., et al (2014). "TNF-alpha-dependent hematopoiesis following Bcl11b deletion in T cells restricts metastatic melanoma" J Immunol 192(4): 1946-1953.
PubMed
Using several tumor models, we demonstrate that mice deficient in Bcl11b in T cells, although having reduced numbers of T cells in the peripheral lymphoid organs, developed significantly less tumors compared with wild-type mice. Bcl11b(-/-) CD4(+) T cells, with elevated TNF-alpha levels, but not the Bcl11b(-/-) CD8(+) T cells, were required for the reduced tumor burden, as were NK1.1(+) cells, found in increased numbers in Bcl11b(F/F)/CD4-Cre mice. Among NK1.1(+) cells, the NK cell population was predominant in number and was the only population displaying elevated granzyme B levels and increased degranulation, although not increased proliferation. Although the number of myeloid-derived suppressor cells was increased in the lungs with metastatic tumors of Bcl11b(F/F)/CD4-Cre mice, their arginase-1 levels were severely reduced. The increase in NK cell and myeloid-derived suppressor cell numbers was associated with increased bone marrow and splenic hematopoiesis. Finally, the reduced tumor burden, increased numbers of NK cells in the lung, and increased hematopoiesis in Bcl11b(F/F)/CD4-Cre mice were all dependent on TNF-alpha. Moreover, TNF-alpha treatment of wild-type mice also reduced the tumor burden and increased hematopoiesis and the numbers and activity of NK cells in the lung. In vitro treatment with TNF-alpha of lineage-negative hematopoietic progenitors increased NK and myeloid differentiation, further supporting a role of TNF-alpha in promoting hematopoiesis. These studies reveal a novel role for TNF-alpha in the antitumor immune response, specifically in stimulating hematopoiesis and increasing the numbers and activity of NK cells.
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Zander, R. A., et al (2015). "PD-1 Co-inhibitory and OX40 Co-stimulatory Crosstalk Regulates Helper T Cell Differentiation and Anti-Plasmodium Humoral Immunity" Cell Host Microbe 17(5): 628-641.
PubMed
The differentiation and protective capacity of Plasmodium-specific T cells are regulated by both positive and negative signals during malaria, but the molecular and cellular details remain poorly defined. Here we show that malaria patients and Plasmodium-infected rodents exhibit atypical expression of the co-stimulatory receptor OX40 on CD4 T cells and that therapeutic enhancement of OX40 signaling enhances helper CD4 T cell activity, humoral immunity, and parasite clearance in rodents. However, these beneficial effects of OX40 signaling are abrogated following coordinate blockade of PD-1 co-inhibitory pathways, which are also upregulated during malaria and associated with elevated parasitemia. Co-administration of biologics blocking PD-1 and promoting OX40 signaling induces excessive interferon-gamma that directly limits helper T cell-mediated support of humoral immunity and decreases parasite control. Our results show that targeting OX40 can enhance Plasmodium control and that crosstalk between co-inhibitory and co-stimulatory pathways in pathogen-specific CD4 T cells can impact pathogen clearance.
Product Citations
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Intratumoral natural killer cells show reduced effector and cytolytic properties and control the differentiation of effector Th1 cells.
In Oncoimmunology on 6 February 2017 by Paul, S., Kulkarni, N., et al.
PubMed
Natural killer (NK) cells are known to have effector and cytolytic properties to kill virus infected or tumor cells spontaneously. Due to these properties, NK cells have been used as an adoptive cellular therapy to control tumor growth in various clinical trials but have shown limited clinical benefits. This indicates that our knowledge about phenotypic and functional differences in NK cells within the tumor microenvironment and secondary lymphoid tissues is incomplete. In this work, we report that B16F10 cell-induced melanoma recruits the CD11b+CD27+ subset of NK cells at a very early stage during tumor progression. These intratumoral NK cells showed increased expression of CD69, reduced inhibitory receptor KLRG1, and decreased proliferative ability. As compared to splenic NK cells, intratumoral NK cells showed decreased expression of activating receptors NKG2D, Ly49D and Ly49H; increased inhibitory receptors, NKG2A and Ly49A; decreased cytokines IFNγ and GM-CSF; decreased cytokine receptors IL-21R, IL-6Rα, and CD122 expression. Depletion of NK cells led to decrease peripheral as well as intratumoral effector CD4+T-bet+ cells (Th1), and increased tumor growth. Furthermore, purified NK cells showed increased differentiation of Th1 cells in an IFNγ-dependent manner. Anti-NKG2D in the culture promoted differentiation of effector Th1 cells. Collectively, these observations suggest that intratumoral NK cells possess several inhibitory functions that can be partly reversed by signaling through the NKG2D receptor or by cytokine stimulation, which then leads to increased differentiation of effector Th1 cells.
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Aged oligodendrocyte progenitors retain the capacity to respond to an inflammatory insult.
In Exp Neurol on 1 October 2026 by Fresenko, E. E., Kaiser, K. E., et al.
PubMed
Aging is associated with neurodegeneration and progressive disability in people living with multiple sclerosis (MS). Aged oligodendrocyte progenitor cells (OPCs) exhibit slower differentiation and remyelination coupled with upregulation of senescence pathways, both in physiological aging and toxin-mediated murine models. The impact of auto-immune demyelinating environment on young and aged OPCs has not been explored. This study combined a genetic OPC lineage tracing approach in young and middle-aged animals with adoptive transfer of MOG-reactive Th17 T cells to determine how aging influences OPC localization, differentiation and remyelination in an autoimmune environment as well as mature oligodendrocyte survival. Lineage traced OPCs were enriched within lesions compared to non-lesion white matter in both age groups and proliferating OPCs were concentrated at lesion edges. Regardless of age, differentiation of lineage traced OPCs into mature OLs was rare and lowest within lesions. Differentiated OLs were reduced in adoptive transfer, particularly in middle-aged animals, and mature OLs were undergoing cell death within lesions and at meningeal borders. Remyelination was present in lesions from both young and middle-aged animals at this acute timepoint. These findings reveal that an autoimmune inflammatory environment stimulated both young and aged OPCs to proliferate near lesion borders, increase their density lesions, undergo differentiation and remyelinate axons. Differentiated OLs were susceptible to cell death within the lesion environment likely due to cytotoxic MOG-reactive T cells. The rapid and robust response of both OPCs in both age groups suggests that autoimmune-mediated demyelination and the inflammatory lesional environment may directly promote OPC recruitment, proliferation, and differentiation. Identifying cell intrinsic pathways in OPCs that promote OPC and newly formed OL survival during an inflammatory challenge will inform the development of remyelination therapies in MS.
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α‑Cyperone targets the PAK1‑JNK/NF‑κB axis to modulate dendritic cells maturation and Th2/Th9 differentiation in an asthma model.
In Int J Mol Med on 1 October 2026 by Hu, H., Wang, X., et al.
PubMed
Asthma is a common chronic airway inflammatory disease affecting millions of patients worldwide, and its treatment remains a clinical challenge. A variety of immune cells, cytokines and inflammatory mediators are associated with asthmatic pathogenesis. The α‑Cyperone (CYP) is the active ingredient of Cyperus rotundus L., which exhibits significant anti‑inflammatory effects in numerous diseases. However, whether and how CYP plays a role in allergic asthma has not yet been reported. It was found that CYP inhibits airway inflammation and mucus hypersecretion in a mouse allergic asthma model by reducing the proportion of mature dendritic cells (DCs) and the differentiation of Th2 and Th9 cells in lung tissue and mediastinal lymph nodes. Furthermore, CYP inhibits DCs maturation via the PAK1‑JNK/nuclear factor‑κB (NF‑κB) pathway, thereby attenuating subsequent Th2 and Th9 cell differentiation. Moreover, it was found that IL‑33 can promote the differentiation of naïve T cells into Th2/Th9 by activating PAK1‑JNK/NF‑κB signaling. CYP decreases this IL‑33‑induced Th2/Th9 differentiation by inhibiting the PAK1‑JNK/NF‑κB axis. The computational analysis indicates that CYP binds to the PAK1 protein at Ser144 that verified by Biacore surface plasmon resonance analyzes and kinase activity testing. Taken together, the present study demonstrated that CYP improves allergic asthma by targeting PAK1 to inhibit the PAK1‑JNK/NF‑κB pathway.
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m6A-Mediated Glycolysis by IL-37 Drives T Cell Metabolic Reprogramming to Regulate Colitis.
In Adv Sci (Weinh) on 1 September 2026 by Wang, X., Yu, J., et al.
PubMed
N6-methyladenosine (m6A) modification and T-cell metabolic reprogramming are increasingly recognized as critical drivers of inflammatory bowel disease (IBD). However, how the anti-inflammatory cytokine interleukin-37 intersects with m6A-mediated metabolic regulation remains unclear. Here, we show that IL-37 alleviates colitis by reducing global m6A levels and reshaping CD4+ T-cell metabolism. Mechanistically, IL-37 signals through its receptor SIGIRR to inhibit IRAK4 and JNK phosphorylation, suppress NF-κB p65 activation, and downregulate METTL14, thereby decreasing m6A deposition. The IL-37/METTL14 axis notably reduces m6A enrichment at the A2445 site in the 3'UTR of SLC2A1, destabilizing its mRNA and suppressing glycolysis. In vitro T-cell polarization and adoptive transfer of METTL14-overexpressing CD4+ T cells confirmed that this metabolic shift restrains Th1/Th17 differentiation while promoting Th2 expansion. Together, these findings reveal the IL-37/SIGIRR-METTL14-m6A axis as a novel regulator of T-cell metabolism and highlight SLC2A1 as a potential therapeutic target in IBD.