Ifnγr1

Manufactured by Jackson ImmunoResearch

Sourced in United States

IFNγR1−/− is a genetically modified mouse strain that lacks the expression of the interferon gamma receptor 1 (IFNγR1) gene. This receptor is a critical component of the signaling pathway for the cytokine interferon gamma, which plays a key role in immune responses. The IFNγR1−/− mouse strain is a valuable tool for researchers studying the specific functions and effects of interferon gamma signaling in various biological processes.

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Lab products found in correlation

Ifn γ, by Jackson ImmunoResearch (2 mentions) C57bl 6j mice, by Jackson ImmunoResearch (2 mentions) Tbx21, by Jackson ImmunoResearch (1 mentions) C57bl 6j wt, by Jackson ImmunoResearch (1 mentions) C57bl 6n, by Jackson ImmunoResearch (1 mentions) C57bl 6j b6, by Jackson ImmunoResearch (1 mentions)

Spelling variants of this product

B6.Ifnγr1−/− (2 citations)

5 protocols using ifnγr1

Murine Malaria Infection Model

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C57BL/6J WT, Il10^−/−, Il10Rβ^−/−, µMT, Tbx21^−/−, and Ifnγr1^−/− (8 weeks old) mice were purchased from Jackson Laboratories. The OUHSC IACUC approved all experiments. Plasmodium yoelii (clone 17XNL, obtained from MR4, ATCC) was routinely passaged through mosquitos. Infections were initiated by a serial transfer of 10⁶P. yoelii parasite-infected red blood cells (pRBCs) i.v. Parasitemia was measured by detecting RNA/DNA content in Ter119⁺ red blood cells via flow cytometry. For IL-10R blockade studies, WT mice were injected i.p. with 200 µg of α-IL-10R (1B1.3A, Bioxcell) or rIgG every three days starting on day 1 p.i. For studies neutralizing IFN-γ, Il10^−/− mice were injected i.p. with 500 µg of α-IFN-γ (XMG1.2, Bioxcell) or rIgG every two days beginning one day prior to infection.

Guthmiller J.J., Graham A.C., Zander R.A., Pope R.L, & Butler N.S. (2016). IL-10 is essential for the generation of germinal center B cell responses and anti-Plasmodium humoral immunity. Journal of immunology (Baltimore, Md. : 1950), 198(2), 617-622.

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Mouse Models for Cancer Immunology

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C57BL/6J mice aged 6 to 8 weeks, RAG2^−/− (#008449), TCRα^−/− (#002116), IFNγ^−/− (#002287), and IFNγR1^−/− (#003288) mice were purchased from Jackson Laboratories. TRP1^high mice (deposited as jax #030958) were previously generated.^{57 (link)} All mice were housed in the Dana-Farber Cancer Institute Animal Resources Facility. Roughly 80% of mice used were females. All animal experiments were performed in accordance with the DFCI IACUC-approved protocols (#14–019 and #14–037) and are in compliance with the NIH/NCI ethical guidelines for tumor-bearing animals.

Walsh M.J., Stump C.T., Kureshi R., Lenehan P., Ali L.R., Dougan M., Knipe D.M, & Dougan S.K. (2023). IFNγ is a central node of cancer immune equilibrium. Cell reports, 42(3), 112219.

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Genetically Engineered Mice for Research

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C57BL/6N and IFNγR1^−/− were obtained from Jackson Laboratories. Dkk3^−/− mice were provided by Niehrs (21 (link)) and backcrossed on C57BL/6N background for more than 10 times. All mice were kept under specific pathogen-free conditions (SPF) at the animal facility of the German Cancer Research Center and used at the age of 8–14 weeks. Animal care was in concordance with the instructions of the regulating authorities.

Meister M., Papatriantafyllou M., Nordström V., Kumar V., Ludwig J., Lui K.O., Boyd A.S., Popovic Z.V., Fleming T.H., Moldenhauer G., Nawroth P.P., Gröne H.J., Waldmann H., Oelert T, & Arnold B. (2015). Dickkopf-3, a Tissue-Derived Modulator of Local T-Cell Responses. Frontiers in Immunology, 6, 78.

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Mouse Models for Cancer Immunology

Cited 1 time

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Walsh M.J., Stump C.T., Kureshi R., Lenehan P., Ali L.R., Dougan M., Knipe D.M, & Dougan S.K. (2023). IFNγ is a central node of cancer immune equilibrium. Cell reports, 42(3), 112219.

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OVA-specific T-cell Transgenic Mouse Model

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Wildtype C57BL/6J (B6), ovalbumin (OVA)-specific T-cell TCR transgenic (OT-II OVA-TCR Tg), iNOS^−/−, IFN-γR1^−/−, GCN2^−/− (B6.129S6) mice were purchased from Jackson Laboratory (Bar Harbor, ME, USA) and used at 10-12 weeks of age. OT-II mice deficient in GCN2 were generated by crossing OT-II mice onto a GCN2 deficient background. All animals were maintained under specific pathogen-free conditions and in accordance with NIH guidelines. All animal procedures were reviewed and approved by the Institutional Animal Care and Use Committee at the Lerner Research Institute.

Bhatt S., Qin J., Bennett C., Qian S., Fung J.J., Hamilton T.A, & Lu L. (2014). All-trans retinoic acid induces Arg-1 and iNOS producing dendritic cells with T cell inhibitory function. Journal of immunology (Baltimore, Md. : 1950), 192(11), 5098-5108.

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