B6.129s7 il1r1tm1imx j

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The B6.129S7-Il1r1tm1Imx/J is a genetically modified mouse strain that lacks the interleukin-1 receptor type 1 (IL-1R1) gene. This strain is commonly used in research to study the role of the IL-1 signaling pathway in various biological processes.

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Il1r1tm1Imx/J (2 citations) IL-1R−/− B6.129S7-Il1r1tm1Imx/J (2 citations)

11 protocols using b6.129s7 il1r1tm1imx j

Characterization of RAG2-deficient SM1 Mice

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RAG2-deficient SM1 CD45.1 mice were produced by backcrossing the original C57BL/6 SM1 RAG2 deficient line to CD45.1 mouse strains (The Jackson Laboratory, Bar Harbor, ME) (42 (link), 43 (link)). IFNγ-eYFP reporter mice (C.129S4(B6)-Ifng^tm3.1Lky/J) were generously provided by R. Lockley, University of California, San Francisco (32 (link)). B6.129S2-Tcra^tm1Mom/J (strain# :002115) and B6.129S7-Il1r1^tm1Imx/J (strain# 003245) were purchased from The Jackson Laboratory and used at 8 to 16 wk of age. All mice were housed in specific pathogen-free conditions and cared for in accordance with the University of California, Davis Institutional Animal Care and Use Committee, and Institutes of Health guidelines.

Depew C.E., Rixon J.A, & McSorley S.J. (2023). Optimal generation of hepatic tissue-resident memory CD4 T cells requires IL-1 and IL-2. Proceedings of the National Academy of Sciences of the United States of America, 120(16), e2214699120.

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Genetically Modified Mouse Strains for Immunology

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Female C57BL/6 (B6) wild-type (WT) mice, B6 albino mice and CD8 T cell deficient mice (H-2Kb/Db KO) on a B6 background were obtained from Taconic farms. B cell deficient mice (μMT/μMT, B6.129S2-Igh-6tm1Cgn/J), and IL-1R1 deficient (B6.129S7-Il1r1tm1Imx/J), were obtained from the Jackson Laboratory (Bar Harbor, ME, United States). IFNγ/Perforin double deficient (IFNγ/Pfp-/-), Perforin deficient (Pfp-/-), CXCR3 deficient (CXCR3-/-) and CXCL10 deficient (CXCL10-/-) mice on a B6 background were produced as previously described (32 (link)) and maintained locally. All mice used in this study were 7 to 14 weeks old and were housed under specific pathogen free (SPF) conditions at the ALAAC accredited animal facility at the Panum Institute (Copenhagen, Denmark). Mice coming from outside sources were allowed to rest for at least 1 week before entering an experiment.

Nazerai L., Schøller A.S., Bassi M.R., Buus S., Stryhn A., Christensen J.P, & Thomsen A.R. (2020). Effector CD8 T Cell-Dependent Zika Virus Control in the CNS: A Matter of Time and Numbers. Frontiers in Immunology, 11, 1977.

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Genetically Modified Mouse Models for Immunology

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C57BL/6J (WT) mice and IL-1R1^-/- (B6.129S7-Il1r1^tm1Imx/J) mice on the C57BL/6 background were purchased from Jackson Laboratories (Bar Harbor, ME) and either bred at the Stanford University Research Animal Facility or used for experiments after maintaining the mice for at least two weeks in our animal facility. C57BL/6-Kit^W-sh/W-sh mice were originally provided by Peter Besmer (Molecular Biology Program, Memorial Sloan-Kettering Cancer Center, New York, NY, USA); we then backcrossed these mice to C57BL/6J mice for more than 11 generations (these mice are available from Jackson Laboratories [B6.Cg-KitW-sh/HNihrJaeBsmGlliJ]). We used age-matched male mice for all experiments. All animal care and experimentation were conducted in compliance with the guidelines of the National Institutes of Health and with the specific approval of the Institutional Animal Care and Use Committees of Stanford University and of the Animal Ethics committee CETEA (Institut Pasteur, Paris, France) registered under #C2EA-89.

Reber L.L., Starkl P., Balbino B., Sibilano R., Gaudenzio N., Rogalla S., Sensarn S., Kang D., Raghu H., Sokolove J., Robinson W.H., Contag C.H., Tsai M, & Galli S.J. (2017). The tyrosine kinase inhibitor imatinib mesylate suppresses uric acid crystal-induced acute gouty arthritis in mice. PLoS ONE, 12(10), e0185704.

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Mice Genetics for Cytokine Signaling

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Eight- to 12-week-old male mice on the C57BL/6 genetic background were
used in all experiments. IL-1α-deficient mice and IL-1β-deficient
mice were a kind gift of Yoichiro Iwakura (University of Tokyo, Japan) and were
generated as previously described^{33 (link)}. Wt C57BL/6 mice, TNF-deficient mice
(B6.129S-^Tnftm1Gkl/J), IL-1R-deficient mice
(B6.129S7-Il1r1^tm1Imx/J) were obtained from Jackson Laboratories
(Bar Harbor, ME). The IL-1R-deficent mice and TNF-deficient mice were crossed to
generate mice deficient in both IL-1R1 and TNF (i.e.,
IL-1R/TNF-deficient mice). The group sizes for each mouse strain included at
least 6 mice/group and a group of 4-5 wt mice were included in every experiment
ensure reproducible results prior to combining data from different iterations.
All mice were bred and maintained under specific pathogen-free conditions at an
American Association for the Accreditation of Laboratory Animal Care
(AAALAC)-accredited animal facility at Johns Hopkins University and were housed
according to procedures described in the Guide for the Care and Use of
Laboratory Animals.

Wang Y., Ashbaugh A.G., Dikeman D.A., Zhang J., Ackerman N.E., Kim S.E., Falgons C., Ortines R.V., Liu H., Joyce D.P., Alphonse M.P., Dillen C.A., Thompson J.M., Archer N.K, & Miller L.S. (2020). IL-1β and TNF are essential in controlling an experimental orthopaedic implant associated infection. Journal of orthopaedic research : official publication of the Orthopaedic Research Society, 38(8), 1800-1809.

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Genetically Modified Mouse Models

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C57BL/6J, IL-1R^−/− (B6.129S7-Il1r1^tm1Imx/J), and IL-18^−/− (B6.129P2-Il18^tm1Aki/J) mice were purchased from The Jackson Laboratories (Bar Harbor, ME). Caspase-1^−/−11^−/− mice were obtained from Dr. Richard A. Flavell (Yale School of Medicine). IL-1α (B6.129-Il1a^tm1Yiw) and IL-1β-deficient mice (B6.129-Il1b^tm1Yiw) on a C57BL/6J background were provided by Dr. Lloyd S. Miller (University of California, Los Angeles) and originally produced by Dr. Yoichiro Iwakura [31] (link). All mice were maintained in specific pathogen-free conditions at the Pennsylvania State University animal care facilities.

Place D.E., Muse S.J., Kirimanjeswara G.S, & Harvill E.T. (2014). Caspase-1-Independent Interleukin-1β Is Required for Clearance of Bordetella pertussis Infections and Whole-Cell Vaccine-Mediated Immunity. PLoS ONE, 9(9), e107188.

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Maintenance and Strain Selection

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Mice were maintained on standard laboratory chow and allowed access to food and water ad libitum. The following strains were used for these experiments: C57Bl6/J, B6.129S7-Il1r1^tm1Imx/J, (Jackson Labs), and CB-17 SCID Beige (Charles River).

Bareja A., Holt J.A., Luo G., Chang C., Lin J., Hinken A.C., Freudenberg J.M., Kraus W.E., Evans W.J, & Billin A.N. (2014). Human and Mouse Skeletal Muscle Stem Cells: Convergent and Divergent Mechanisms of Myogenesis. PLoS ONE, 9(2), e90398.

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Diverse Transgenic Mouse Models

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C57BL/6, B6.Cg-Tg(Cd4-TGFBR2)16Flv/J, B6.129S2-Irf1^tm1Mak/J, B6.Cg-Tg(TcraTcrb)425Cbn/J, B6.129S7-Il1r1^tm1Imx/J, and B6.Cg-Rag1^tm1MomTyrp1^B-w Tg(Tcra,Tcrb)9Rest/J mice were purchased from The Jackson Laboratory. Male and female 6–8-week-old mice were used for each animal experiment. All experiments complied with protocols approved by the Institutional Animal Care and Use Committee at the Wake Forest School of Medicine.

Xue G., Jin G., Fang J, & Lu Y. (2019). IL-4 together with IL-1β induces antitumor Th9 cell differentiation in the absence of TGF-β signaling. Nature Communications, 10, 1376.

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Mice Strains for Neuroscience Research

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We used female C57BL/6J (WT, n = 162), B6.129S7-Il1r1tm1Imx/J (IL1R1^−/−, n = 28) and apolipoprotein E–deficient (ApoE^−/−; B6.129P2-Apoetm1Unc/J, n = 24) mice aged 8–12 weeks (The Jackson Laboratories, Bar Harbor, ME, USA) for our studies. We also used transgenic mice expressing green fluorescent protein (GFP) under the Nestin-promoter (Nestin-GFP, n = 10)^{26 (link), 27 (link)}. Nestin-GFP mice were a gift from Dr. Grigori Enikolopov (Cold Spring Harbor Laboratory, NY, USA). Age-matched mice were randomly allocated either to control or treatment groups. The study was approved by the Subcommittee on Animal Research Care at Massachusetts General Hospital (Boston, MA).

Sager H.B., Heidt T., Hulsmans M., Dutta P., Courties G., Sebas M., Wojtkiewicz G.R., Tricot B., Iwamoto Y., Sun Y., Weissleder R., Libby P., Swirski F.K, & Nahrendorf M. (2015). Targeting Interleukin-1β Reduces Leukocyte Production After Acute Myocardial Infarction. Circulation, 132(20), 1880-1890.

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Mice Strains for Immunological Studies

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BALB/c, C57BL/6, C.C3-Tlr4^Lps-d/J (Tlr4^-d), C.129-Il4^tm1Lky/J (4get), Tg(Cd4-cre)1Cwi/BfluJ (Cd4-Cre), B6.129P2-Tcrb^tm1Mom/J (Tcrb^−/−), B6Cr.129S4-Tnfsf4^tm1Sug/Pgn (Tnfsf4^−/−), B6;129S1-Il1rap^tm1Roml/J (Il1rap^−/−), and B6.129S7-Il1r1^tm1Imx/J (Il1r^−/−) mice were obtained from The Jackson Laboratory (Bar Harbor, ME, USA). Il1rap^−/− mice were subsequently backcrossed onto the BALB/c background for 10 generations. Il1rl1^−/− (ST2^−/−) mice and Crlf2^−/− (Tslpr^−/−) mice (both BALB/c background) were kindly provided by Dr. Andrew McKenzie (MRC Laboratory of Molecular Biology, Cambridge, UK) and Dr. Steven F. Ziegler (Benaroya Research Institute, Seattle, WA, USA), respectively, and were bred under specific pathogen-free (SPF) conditions at the Mayo Clinic (Rochester, MN, USA)^{21 (link), 22 (link)}. Bcl6^fl/fl mice were previously described^{23 (link)}. Animals used in this study were female and ranged from 6–12 weeks of age. All protocols and procedures for handling of the mice were reviewed and approved by the Mayo Institutional Animal Care and Use Committee, Mayo Clinic.

Dolence J.J., Kobayashi T., Iijima K., Krempski J., Drake L.Y., Dent A.L, & Kita H. (2017). Airway exposure initiates peanut allergy by involving the IL-1 pathway and T follicular helper cells in mice. The Journal of allergy and clinical immunology, 142(4), 1144-1158.e8.

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Conditional Knockout Mice Generation

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Founder mice utilized in this study were purchased from The Jackson Laboratory (Bar Harbor, Maine) and included the following strains: C57BL/6J (Cat #000664), B6.129S7-Rag1tm1Mom/J (RAG1 Knockout (KO), Cat # 002216), B6.Cg-Tg(TcraTcrb)425Cbn/J (OT-II, Cat # 004194), B6.129S2-Cd4tm1Mak/J (CD4 KO, Cat# 002663), B6.129S7-Il1r1^tm1Imx/J (IL-1R KO, Cat# 003245), B6.129P2-Lyz2tm1(cre)Ifo/J (Lyz2-Cre, Cat # 004781), B6.Cg-Tg(Cd4-cre)1Cwi/BfluJ (CD4-Cre, Cat # 022071) and B6.129P2(SJL)-Myd88tm1Defr/J (MyD88^Flox/Flox, Cat # 008888). While CD4-Cre.MyD88^Flox/Flox conditional KO mice were generated by crossing CD4-Cre mice with MyD88^Flox/Flox mice (resulting in Cre-mediated excision of MyD88 in CD4+ as well as CD8+ T-cells), Lyz2-Cre.MyD88^Flox/Flox conditional KO mice were produced by crossing Lyz2-Cre mice with MyD88 ^Flox/Flox mice—resulting in excision of MyD88 in cells of myeloid lineage. For each strain, F1 WT/Cre-WT/FL mice were crossed to produce WT/Cre-FL/FL mice. Backcrossing of F1 WT/Cre-FL/FL mice to WT/WT-FL/FL mice yielded additional WT/Cre-FL/FL experimental mice. All mice were genotyped prior to breeding/experimental use. Mice were provided with food and water ad libitum and housed in specific pathogen free mouse facilities under IACUC-approved protocols (University of Pittsburgh, Pittsburgh, PA).

Reay D.P., Tabib T., Wang Y., Oriss T.B., Young N.A., Lafyatis R.A., Jarjour W.N., Clemens P.R, & Ascherman D.P. (2023). Antigen-driven T cell-macrophage interactions mediate the interface between innate and adaptive immunity in histidyl-tRNA synthetase-induced myositis. Frontiers in Immunology, 14, 1238221.

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