Il 18r

Manufactured by Jackson ImmunoResearch

Sourced in United States

IL-18R(−/−) is a lab equipment product that functions as a knockout mouse model. It is a genetically modified mouse strain that lacks the expression of the interleukin-18 receptor (IL-18R) gene.

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6 protocols using il 18r

Generation of Genetically Modified Mice

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MyD88^(−/−) (Stock No. 009088, Jackson Laboratories) and CARD9^(−/−) [69 (link)] were crossed to generate MyD88^(−/−)CARD9^(−/−) mice. IL-1R^(−/−) (Stock No. 003245), IL-18R^(−/−) (Stock Number 004131), C57BL/6 (CD45.2⁺), C57BL/6.SJL (CD45.1⁺), mice were from Jackson Laboratories. TLR2^(−/−) and TLR4^(−/−) mice were obtained by the Pamer laboratory from the Medzhitov laboratory in 2000 and backcrossed at least 10 generations on the C57BL/6 background. All mouse strains were bred and housed in the FHCRC Comparative Medicine Shared Resources or in the MSKCC Research Animal Resource Center under specific pathogen-free conditions. MyD88^{(−/−)CC10-MyD88} [33 (link)] and non-transgenic MyD88^(−/−) littermate controls were bred and maintained at the Yale University Animal Resources Center and shipped to MSKCC for experimental use.

Jhingran A., Kasahara S., Shepardson K.M., Junecko B.A., Heung L.J., Kumasaka D.K., Knoblaugh S.E., Lin X., Kazmierczak B.I., Reinhart T.A., Cramer R.A, & Hohl T.M. (2015). Compartment-Specific and Sequential Role of MyD88 and CARD9 in Chemokine Induction and Innate Defense during Respiratory Fungal Infection. PLoS Pathogens, 11(1), e1004589.

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Immunization of Mice with ID93 and rHA

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Female wild-type (WT) C57BL/6, NLRP3^-/-, and IL-18R^-/- mice aged 6–10 weeks were purchased from the Jackson Laboratory. ASC^-/- were a kind gift of Amy Hise (Case Western Reserve University, USA) and were bred in-house. All strains were on the C57BL/6 background and maintained in Specific Pathogen Free conditions. All animal experiments and protocols used in this study were approved by the Infectious Disease Research Institute’s Institutional Animal Care and Use Committee. Mice were immunized twice, 3 weeks apart via an intramuscular injection in the calf muscles of hind limb with 0.5 µg of ID93 or 0.1 µg rHA recombinant protein.^{48 (link)} Adjuvants were added as follows per dose: SE (2%), SLA (5 µg), Alhydrogel (100 µg aluminum) nanoalum (100 µg aluminum), and/or PAA (2.7 µg). For innate immune responses, draining inguinal lymph nodes were collected 6 h after immunization. For adaptive immune responses, spleens were collected in RPMI 7 days after the second immunization. Cells suspensions were obtained by manual disruption. Red blood cells contained in spleens were lysed using the Red Blood Cell Lysis Buffer (ThermoFisher). Total viable cells were counted (Guava Technologies, Millipore) and plated at 2 × 10⁶ cells/well in round-bottom 96-well plates.

Orr M.T., Khandhar A.P., Seydoux E., Liang H., Gage E., Mikasa T., Beebe E.L., Rintala N.D., Persson K.H., Ahniyaz A., Carter D., Reed S.G, & Fox C.B. (2019). Reprogramming the adjuvant properties of aluminum oxyhydroxide with nanoparticle technology. NPJ Vaccines, 4, 1.

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Mouse Strains for Rotavirus Research

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All mice used herein were adults (i.e. 4–8 week-old) on a C57BL/6 background bred at Georgia State University (Atlanta, GA). Rotavirus-infected mice were housed in an animal biosafety level 2 facility. WT, Rag-1^−/−, IL-18^−/−, IL-18-R^−/−, Stat3^flox, and Villin-cre were purchased from Jackson Laboratories (Bar Harbor, ME, USA). NLRC4^−/−, IL-22^−/−, and IL-22-R^−/− mice were provided by Genentech (South San Francisco, CA, USA). TLR5^−/− and TLR5^−/−/NLRC4^−/− and WT littermates were maintained as previously described (5 (link)). Gasdermin D/E^−/− mice, whose generation and initial characterization was previously described (22 (link)) were shipped to GSU and studied in original and cross-fostered state as indicated in results.

Zhang Z., Zou J., Shi Z., Zhang B., Etienne-Mesmin L., Wang Y., Shi X., Shao F., Chassaing B, & Gewirtz A.T. (2020). IL-22 induced cell extrusion and IL-18-induced cell death prevent and cure rotavirus infection. Science immunology, 5(52), eabd2876.

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Murine Models for Immunology Research

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C57BL/6J WT, BALB/c WT, TLR4 mutant (C3HeJ), Tlr4^−/−, Il18r^−/−, Il12p40^−/−, Tlr2^−/−, Tlr5^−/−, Il1r1^−/−, Il12p35^−/−, Langerin-eGFP-DTR, Cd11c-Cre, and B6.SJL-Ptprc^aPep3^b/BoyJ (OT-II) transgenic mice were purchased from the Jackson Laboratory. C3HeB/FeJ mice were purchased from Taconic. DO11.10 TCR transgenic mice were purchased from Charles River Laboratory. Myd88^−/−, Trif^−/− (Hise et al., 2007 (link)), Il22^−/− (Zheng et al., 2007 (link)), IIl23r^−/− (Chan et al., 2006 (link)), Unc93b1^−/− (Kim et al., 2008 (link); provided by H. Ploegh, Whitehead Institute for Biomedical Research, Cambridge, MA), Il23p19^−/− (Edgerton et al., 2009 (link); provided by M. Oukka, Center of Immunity and Immunotherapies, Seattle Children's Research Institute, Seattle, WA), and Il1rl1^−/− mice (Barlow et al., 2013 (link)) were previously described. All mice were kept in a pathogen-free environment and fed an OVA-free diet. GF mice were bred at the gnotobiotic Research Animal Facility at The University of Chicago. All procedures performed on the mice were in accordance with the Animal Care and Use Committee of the Children's Hospital Boston.

Yoon J., Leyva-Castillo J.M., Wang G., Galand C., Oyoshi M.K., Kumar L., Hoff S., He R., Chervonsky A., Oppenheim J.J., Kuchroo V.K., van den Brink M.R., Malefyt R.D., Tessier P.A., Fuhlbrigge R., Rosenstiel P., Terhorst C., Murphy G, & Geha R.S. (2016). IL-23 induced in keratinocytes by endogenous TLR4 ligands polarizes dendritic cells to drive IL-22 responses to skin immunization. The Journal of Experimental Medicine, 213(10), 2147-2166.

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Genetically Modified Murine Models for Immunological Research

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C57BL/6, B6.SJL- Ptprc^aPepcb/BoyJ, B6.PL-Thy1a/CyJ, Cd4-cre, Myd88^fl/fl, IL-18R-deficient, IL-15R-deficient mice were purchased from The Jackson Laboratory at 6–8 weeks of age. DR3-deficient mice [65 (link)], were maintained at the University of Southampton. T cell-specific MyD88-deficient mice were generated for this study by intercrossing Cd4-cre mice and Myd88^fl/fl mice. All mice were genotyped before use by PCR according to protocols provided by The Jackson Laboratory. CD90.1 RAG-deficient SM1 TCR transgenic mice were bred at UC Davis and assessed by flow cytometry [45 (link),66 ].

Pham O.H., O’Donnell H., Al-Shamkhani A., Kerrinnes T., Tsolis R.M, & McSorley S.J. (2017). T cell expression of IL-18R and DR3 is essential for non-cognate stimulation of Th1 cells and optimal clearance of intracellular bacteria. PLoS Pathogens, 13(8), e1006566.

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Genetically Modified Mice for Immunology

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C57BL/6, B6.SJL-Ptprc^aPepc^b/BoyJ, B6.PL-Thy1^a/CyJ, TLR4-deficient, and IL-18R-deficient mice were purchased from The Jackson Laboratory or NCI at 6–8 weeks of age. MyD88-, IL-1R1-, and IFN-γR-deficient C57BL/6 mice were obtained from Dr. Jenkins (University of Minnesota) and Dr. Way (University of Cincinnati), and bred in our animal facility. IL-33R-deficient C57BL/6 mice were kindly provided by Dr. Bryce (Northwestern University). Mice deficient in NLRC4 and NLRP3 were maintained at Stanford University (Broz et al., 2010 (link)). T cell specific Myd88 deficient mice were generated by crossing Lck-cre mice to Myd88^flox/flox flanked mice purchased from Jackson labs. Mice were genotyped by PCR according to protocols provided by The Jackson Laboratory. All animal procedures were approved by UC Davis IACUC (#16612).

O’Donnell H., Pham O.H., Li L.X., Atif S.M., Lee S.J., Ravesloot M.M., Stolfi J.L., Nuccio S.P., Broz P., Monack D.M., Baumler A.J, & McSorley S.J. (2014). Toll-like receptor and inflammasome signals converge to amplify the innate bactericidal capacity of T helper-1 cells. Immunity, 40(2), 213-224.

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