B6.129p2 lyz2tm1 cre ifo j

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B6.129P2-Lyz2tm1(cre)Ifo/J is a laboratory mouse strain that expresses Cre recombinase under the control of the lysozyme 2 (Lyz2) gene promoter. The Lyz2 gene is expressed in monocytes and macrophages, allowing for the specific deletion or modification of target genes in these cell types.

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LysM-Cre (B6.129P2-Lyz2tm1(cre)Ifo/J) mice (13 citations) B6.129P2-Lyz2tm1(cre)Ifo/J (LysMcre, (9 citations) B6.129P2-Lyz2tm1(cre)Ifo/J mice (6 citations) (B6N.129P2(B6)-Lyz2tm1(cre)Ifo/J, (3 citations) B6.129P2-Lyz2tm1(cre)Ifo, (2 citations) B6.129P2-Lyz2tm1(cre) (2 citations) Strain B6.129P2-Lyz2tm1(cre)Ifo/J (2 citations)

54 protocols using b6.129p2 lyz2tm1 cre ifo j

Genetic Targeting of Myeloid Cells

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Lyz2cre/cre (B6.129P2-Lyz2^tm1⁽^cre⁾^Ifo/J The Jackson Laboratory) and Lyz2cre/cre Hif1α^fl/fl mice were housed in isolator cages and maintained by the Department of Laboratory Animal Medicine, University of Cincinnati, accredited by the Association for Assessment and Accreditation of Laboratory Animal Care. For the Ldha experiments (Fig. 2E and F), Lyz2cre/cre Ldha^fl/fl mice [B6(Cg)-Ldha^tm1c⁽^EUCOMM⁾^Wtsi/DatsJ; The Jackson Laboratory] and Lyz2cre/cre (B6.129P2-Lyz2^tm1⁽^cre⁾^Ifo/J; The Jackson Laboratory) control mice were housed in isolator cages and maintained by the Division of Veterinary Services at Cincinnati Children’s Hospital Medical Center (CCHMC), accredited by the Association for Assessment and Accreditation of Laboratory Animal Care. All animal experiments were performed in accordance with the Animal Welfare Act guidelines of the National Institutes of Health, and all protocols were approved by the Institutional Animal Care and Use Committees of the University of Cincinnati or CCHMC.

Evans H.M., Schultz D.F., Boiman A.J., McKell M.C., Qualls J.E, & Deepe GS J.r. (2021). Restraint of Fumarate Accrual by HIF-1α Preserves miR-27a-Mediated Limitation of Interleukin 10 during Infection of Macrophages by Histoplasma capsulatum. mBio, 12(6), e02710-21.

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Genetically Modified Mouse Model Comparison

Cited 2 times

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Wildtype (C57BL/6J), Ripk1^K45A/K45A (indicated as Ripk1^KD/KD [kinase-dead]) (Berger et al, 2014 (link)), Ripk3^−/− (Newton et al, 2004 (link)), Mlkl^−/− (Murphy et al, 2013 (link)), Lyz2^creMap3k7^fl/fl (indicated as Tak1^fl/fl) conditional knockout (generated by crossing B6.129P2-Lyz2^tm1(cre)Ifo/J [The Jackson Laboratory] and Tak1^fl/fl) (Xie et al, 2006 (link)), and Lyz2^creDdx3x^fl/fl (generated by crossing B6.129P2-Lyz2^tm1(cre)Ifo/J [The Jackson Laboratory] and Ddx3x^fl/fl) (Samir et al, 2019 (link)) mice were maintained on the B6 background. Male and female mice were used in this study at 6–10 wk of age. Mice were bred at St. Jude Children’s Research Hospital, and studies were conducted under protocols approved by St. Jude Children’s Research Hospital Committee on the Use and Care of Animals.

Place D.E., Samir P., Malireddi R.S, & Kanneganti T.D. (2021). Integrated stress response restricts macrophage necroptosis. Life Science Alliance, 5(1), e202101260.

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Conditional Knockout Mice for Metabolism

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Gls1^fl/fl mice were kindly provided by Pr. Stephen Rayport (Glstm2.1Sray/J deposited at The Jackson Laboratory) and have been crossed to Lyz2^Cre mice (B6.129P2-Lyz2tm1(cre)Ifo/J, The Jackson Laboratory) or Mx1^cre mice (B6.Cg-Tg(Mx1-cre)1Cgn/J) and brought on Apoe-deficient genetic background (B6.129P2-ApoEtm1Unc/J). Mx1^cre mice (B6.Cg-Tg(Mx1-cre)1Cgn/J) were also crossed to C57BL/6 Glud1 floxed mice (kindly provided by Pr. Pierre Maechler). For each experiment, co-housed littermate male and female controls were used between eight and fourteen weeks of age. Animal protocols were approved by the Institutional Animal Care and Use Committee of the French Ministry of Higher Education and Research and the Mediterranean Center of Molecular Medicine (Inserm U1065) and were undertaken in accordance with the European Guidelines for Care and Use of Experimental Animals. Animals had free access to food (chow diet A04, Safe^R) and water and were housed in a controlled environment with a 12-hour light–dark cycle, constant temperature (21.7-22.8°C) and relative humidity (50-60%). Water and cages were autoclaved. Cages were changed once weekly, and the health status of the mice was monitored using a dirty bedding sentinel program. Hyperlipidemia was induced by feeding the mice with a Western diet (TD88137, Ssniff) for 12 weeks.

Merlin J., Ivanov S., Dumont A., Sergushichev A., Gall J., Stunault M., Ayrault M., Vaillant N., Castiglione A., Swain A., Orange F., Gallerand A., Berton T., Martin J.C., Carobbio S., Masson J., Gaisler-Salomon I., Maechler P., Rayport S., Sluimer J.C., Biessen E.A., Guinamard R.R., Gautier E.L., Thorp E.B., Artyomov M.N, & Yvan-Charvet L. (2021). Non-canonical glutamine transamination sustains efferocytosis by coupling redox buffering to oxidative phosphorylation. Nature metabolism, 3(10), 1313-1326.

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Conditional Knockout of Irf6 in Myeloid Cells

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All animal procedures were approved by the University of Iowa Institutional Animal Care and Use Committee protocol 5011268. Male and female (8–12 weeks old) C57Bl/6, LysM^Cre knock-in (B6.129P2-Lyz2^tm1(cre)Ifo/J, stock 004781;Jackson Laboratories, Bar Harbor, ME, USA), and Irf6^fl (generous gift from Brian Schutte, Michigan State University, USA) were used. LoxP sites were located in introns 2 and 4 of the Irf6 gene. Recombination excised exons 3 and 4, which deleted part of the DNA binding domain. This is an Irf6 null (nl) allele as mice that are homozygous for this deletion have the expected null phenotype (Kinoshita and Schutte, personal communication). Crosses between Irf6^fl/fl or Irf6^fl/nl and LysM^Cre lead to LysM^Cre;Irf6^fl/fl or LysM^Cre;Irf6^fl/nl, named Irf6 cKO hereafter. Irf6^fl/fl or Irf6^+/+ will be considered wild type.

Joly S., Rhea L., Volk P., Moreland J.G, & Dunnwald M. (2016). Interferon Regulatory Factor 6 Has a Protective Role in the Host Response to Endotoxic Shock. PLoS ONE, 11(4), e0152385.

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Genetically Modified Mouse Strains

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Mice were housed in the Center for Comparative Physiology at the Feinstein Institutes for Medical Research. C57BL/6 (B6) and B6.C-H2d/bByJ (B6.H2^d) mice were purchased from The Jackson Laboratory. RAGE KO mice were a generous gift from Kevin Tracey, MD, of the Feinstein Institutes for Medical Research. LAIR-1 cKO mice were generated by crossing B6.129P2-Lyz2^tm1(cre)Ifo/J with B6.Cg-Lair1^tm1Jco/J (The Jackson Laboratory) after backcrossing onto the B6.H2^d background. B6.Cg-Tg(Camk2a-cre)T29–1Stl/J and Hmgb1^tm1.1Rshw/J (Jackson Laboratories) were crossed with in house B6.H2^d mice to generate Camk2a-cre HMGB1^fl/fl B6.H2^d mice. All procedures using mice were conducted using protocols approved by The Feinstein Institutes of Medical Research IACUC (Protocols 2009–048 and 2022–023).

Carroll K.R., Mizrachi M., Simmons S., Toz B., Wingard J., Tehrani N., Zarfeshani A., Kello N., Kowal C., Levin J.Z., Volpe B.T, & Diamond B. (2023). Lupus autoantibodies initiate a maladaptive equilibrium sustained by HMGB1:RAGE signaling and reversed by LAIR-1:C1q signaling. Research Square.

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Conditional Mapk8 Knockout Mice

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All experiments were performed on age-matched (from 8 to 12 weeks of age) female mice. Wild type C57Bl/6 mice were purchased from Envigo. Mapk8^fl/fl mice (C57BL/6 background) were previously described (9 (link)) and kindly provided by Thomas Wunderlich and Jens Brüning, Institute for Genetics, University of Cologne. B6.C-Tg(Pgk1-cre)1Lni/CrsJ (stock 020811), B6.129P2-Lyz2tm1(cre)Ifo/J (stock 004781), B6N.Cg-Tg(KRT14-cre)1Amc/J (stock 018964) and B6.Cg-Tg(Itgax-cre)1-1Reiz/J (stock 008068) mice were obtained from the Jackson Lab. Littermates were used as controls in all experiments. All mice were bred and maintained in a conventional animal facility.

Le A., Azouz A., Thomas S., Istaces N., Nguyen M, & Goriely S. (2021). JNK1 Signaling Downstream of the EGFR Pathway Contributes to Aldara®-Induced Skin Inflammation. Frontiers in Immunology, 11, 604785.

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Transgenic Mouse Models in Immunology

Cited 2 times

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MRP8-Cre/iresGFP mice (B6.Cg-Tg(S100A8-cre,-EGFP)1Ilw/J; Passegué et al., 2004 (link); Reber et al., 2017a (link)) were obtained from Irving Weissman (Stanford University, Stanford, CA) and Clifford Lowell (University of California, San Francisco, San Francisco, CA). Kit^W-sh/W-sh mice (B6.Cg-Kit^W-sh/HNihrJaeBsmGlliJ), Lys-Cre mice (B6.129P2-Lyz2^tm1(cre)Ifo/J), and Cd11c-Cre mice (B6.Cg-Tg(Itgax-cre)1-1Reiz/J) were obtained from The Jackson Laboratory. C57BL/6-Mcpt5-Cre⁺ mice (Dudeck et al., 2011 (link)) were provided by A. Roers. NLRP3^A350VneoR (B6.129-Nlrp3^tm1Hhf/J) and Nlrp3^L351PneoR mice (B6N.129-Nlrp3^tm2Hhf/J) have been described previously (Brydges et al., 2009 (link)). Mice were bred in the Institut Pasteur; University of California, San Diego; or Stanford University specific pathogen–free animal facilities. 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 the University of California, San Diego, and/or of the Committee for Ethics in Animal Experimentation (Institut Pasteur, Paris, France) registered under #C2EA-89.

Stackowicz J., Gaudenzio N., Serhan N., Conde E., Godon O., Marichal T., Starkl P., Balbino B., Roers A., Bruhns P., Jönsson F., Moguelet P., Georgin-Lavialle S., Broderick L., Hoffman H.M., Galli S.J, & Reber L.L. (2021). Neutrophil-specific gain-of-function mutations in Nlrp3 promote development of cryopyrin-associated periodic syndrome. The Journal of Experimental Medicine, 218(10), e20201466.

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ADAR1 Knockout Mice in Disease Models

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ADAR1 knockout mice (B6.129(Cg)-Adartm1.1Phs/KnkMmjax), ADAR1fl/fl mice (B6.129-Adartm1Knk/Mmjax), and LysM-cre mice (B6.129P2-Lyz2tm1(cre)Ifo/J) were purchased from the Jackson Laboratory (Bar Harbor, ME). Mice aged 6-8 weeks were used for analyses in this study. All mice were housed under conventional conditions in the animal care facilities by the Xi’an Jiaotong University Division of Laboratory Animal Research. All animal procedures were approved by the Institutional Animal Care and Use Committee of Xi’an Jiaotong University, Xi’an Center for Disease Control.

Sun C., Cai D, & Chen S.Y. (2022). ADAR1 promotes systemic sclerosis via modulating classic macrophage activation. Frontiers in Immunology, 13, 1051254.

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TLR4 Knockout Mice for Myeloid Cell Studies

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Adult mice from 8 to 10 weeks were used to perform the experiments. Different genotypes of mice were used. WT mice (B6.C57BL/6J) were obtained from Harlan. To elucidate the specific role of TLR4 in different cells transgenic mice expressing the Cre recombinase enzyme under the lysozyme M promoter were used (B6.129P2-Lyz2tm1(cre)Ifo/J, Jackson Laboratory). Those animals were crossed with TLR4^loxP/loxP mice, kindly donated by Prof. Timothy Billiar (University of Pittsburgh, USA) to obtain mice lacking TLR4 specifically in myeloid cells (TLR4 lack of expression was routinely checked by qPCR resulting in a TLR4 expression similar to the one detected in TLR4 full knock-out mice). Mice had access to rodent chow and water ad libitum in a 12 h light/dark cycle room. All groups were performed and quantified in a randomized fashion by investigators blinded to the specific treatments. All procedures were performed in accordance with the European Parliament and of the Council Directive 2010/63/EU and Spanish legislation (RD 53/2013) and were approved by the Ethics Committee on Animal Welfare of University Complutense (PROEX number 016/18) and are reported according to ARRIVE guidelines (Animal Research: Reporting of In Vivo Experiments).

Durán-Laforet V., Peña-Martínez C., García-Culebras A., Cuartero M.I., Lo E.H., Moro M.Á, & Lizasoain I. (2021). Role of TLR4 in Neutrophil Dynamics and Functions: Contribution to Stroke Pathophysiology. Frontiers in Immunology, 12, 757872.

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Conditional gene knockout mouse models

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8–12 weeks old mice were used. C57BL/6J (Strain #000,664), B6.129S4(C)-Vhltm1Jae/J (Vhl^fl/fl) (Strain #012933), B6.129X1-Nfe2l2tm1Ywk/J (Nfe2l2^−/−) (Strain #017009), B6.129P2-Lyz2tm1(cre)Ifo/J (Strain #004781), B6.129P2-Nos2tm1Lau/J (Nos2^−/−) (Strain # 002609) and B6.129S-Cybbtm1Din/J (Cybb^−/−) (Strain #002365) mice were purchased from The Jackson Laboratory. Nfe2l2^−/− mice were generated by first crossing with WT C57BL/6J mice, followed by heterozygote intercrossing. Lyz2-Cre:Vhl^fl/fl mice were generated by backcrossing a single Lyz2-Cre transgene into Vhl^fl/fl mice. Breeding for experiments consisted of crosses between Cre-positive and Cre-negative Vhl^fl/fl mice. All mice were maintained in a pathogen-free, temperature-regulated environment with a 12-h light and dark cycle. All mice used in comparative studies were age-matched, with littermates used as controls. In terms of mouse sexes, both male and female mice were used. Apart from C57BL/6J, all mice were sex-matched across genotypes (Cre-positive and Cre-negative littermates). All mice were fed a normal chow diet (NCD, 16 kcal% fat). All studies were performed under the approval of Animal User Protocols by the Animal Care Committee at the University Health Network according to the guidelines of the Canadian Council on Animal Care. The results in this study were reported in accordance with ARRIVE guidelines.

Ting K.K., Yu P., Dow R., Ibrahim H., Karim S., Polenz C.K., Winer D.A., Woo M., Jongstra-Bilen J, & Cybulsky M.I. (2024). Cholesterol accumulation impairs HIF-1α-dependent immunometabolic reprogramming of LPS-stimulated macrophages by upregulating the NRF2 pathway. Scientific Reports, 14, 11162.

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