Rag1tm1mom

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Rag1tm1Mom is a genetically engineered mouse strain that carries a targeted mutation in the Rag1 gene. This mutation disrupts the normal function of the Rag1 protein, which is essential for the development of T cells and B cells in the immune system. The Rag1tm1Mom mouse strain is commonly used in immunological research to study the role of the Rag1 gene in immune system development and function.

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13 protocols using rag1tm1mom

Mouse Strains for Immunological Studies

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C57BL/6 wild-type control mice were obtained from the UT Southwestern Mouse Breeding Core Facility. IL-1β^−/− mice were generated by David Chaplin, UA at Birmingham and provided to us by Fayyaz S. Sutterwala at Cedars Sinai. Rip3^−/− and Rip3^−/−Casp8^−/− mice were provided by Andrew Oberst at the University of Washington. ASC KO mice were a gift from Genentech. Gsdmd^−/− mice were provided by Jonathan Kagan at Boston Children’s Hospital. Caspase-1 KO were provided by Russell Vance at University of California, Berkeley. B6.MRL-Fas^lpr/J (lpr), B6.129S-Tnf^tm1Gkl/J (Tnfa^−/−), B6.129S-Tnfrsf1a^tm1ImxTnfrsf1b^tm1Imx/J (Tnfrsf1a/b^−/−), Rag1^tm1Mom, Casp1/11^null, 2D2 TCR transgenic mice and Zbtb46^gfpwere obtained from Jackson Laboratories. All mice were bred and housed in a specific pathogen-free facility at UT Southwestern Medical Center and Cincinnati Children’s Hospital Medical Center. For isolation of steady state CD4 memory T cells, mice were housed in a conventional facility for 2–4 weeks before tissue isolation. All mouse experiments were done as per protocols approved by Institutional Animal Care and Use Committee (IACUC) at UT Southwestern Medical Center and Cincinnati Children’s Hospital Medical Center.

Jain A., Irizarry-Caro R.A., McDaniel M.M., Chawla A.S., Carroll K.R., Overcast G.R., Philip N.H., Oberst A., Chervonsky A.V., Katz J.D, & Pasare C. (2019). T cells instruct myeloid cells to produce inflammasome-independent IL-1β and cause autoimmunity. Nature immunology, 21(1), 65-74.

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Fecal Sample Preservation for Microbiome

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Fresh fecal pellets were collected from adult WT C57BL/6J (Stock #000664; Jackson Laboratory) and Rag1^tm1Mom (Stock #002216; Jackson Laboratory) mice, pooled by genotype, and stored at −80°C. Mouse fecal pellets were thawed and resuspended in 10 ml of BIOME-preserve anaerobic medium, transferred to a gentleMACS C tube (Miltenyi), and homogenized via gentleMACS Dissociator (Miltenyi) for three cycles of 61 s on the “intestine” setting. All stool homogenates were aliquoted into 2.0-ml cryovials (VWR) and stored at −80°C.

Scheid J.F., Eraslan B., Hudak A., Brown E.M., Sergio D., Delorey T.M., Phillips D., Lefkovith A., Jess A.T., Duck L.W., Elson C.O., Vlamakis H., Plichta D.R., Deguine J., Ananthakrishnan A.N., Graham D.B., Regev A, & Xavier R.J. (2023). Remodeling of colon plasma cell repertoire within ulcerative colitis patients. The Journal of Experimental Medicine, 220(4), e20220538.

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Genetically Modified Mice for Immunological Studies

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All male and female mice used for experiments were between 6 and 12 weeks old; age-matched littermates were used. The RORγt^−/− (Rorc^tm1Litt, stock no. 007571) mouse strain was described previously (18 (link)). The RORγt^K256R/K256R point-mutated mice were designed and generated by Biocytogen LLC. Rag1^−/− (Rag1^tm1Mom, stock no. 002216), Tg^Tcr2D2 (Tcra2D2 and Tcrb2D2, stock no. 006912), IL-17A–GFP (Il17a^tm1Bcgen, stock no. 018472), CRISPR-Cas9– enhanced GFP (EGFP) [Gt(ROSA)26Sor^{em1.1(CAG-cas9}*^,-EGFP)Rsky, stock no. 028555], and C57BL/6J (stock no. 000664) mice were purchased from the Jackson Laboratory. For some assays, the mice were crossed to generate RORγt^−/−/Tg^Tcr2D2, RORγt^K256R/K256R/Tg^Tcr2D2, and RORγt^K256R/K256R/IL-17A-IRES-GFP-KI mice. All mice were bred at the C57BL/6J background and maintained in a pathogen-free animal facility at City of Hope. All animal experiments were conducted per the protocols approved by the Institutional Animal Care and Use Committee at City of Hope. Statistical tests were not used to predetermine sample sizes. The sample sizes were chosen on the basis of previous studies of our own and by others in the field (8 (link)). The sample sizes are indicated in the figure legends or figures. Allocation of mice to experimental groups was random.

Zhong X., Wu H., Zhang W., Gwack Y., Shang W., Lee K.O., Isakov N., He Z, & Sun Z. (2022). Decoupling the role of RORγt in the differentiation and effector function of TH17 cells. Science Advances, 8(42), eadc9221.

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Amelioration of Colitis in Humanized Mice

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Example 11

The ability of the BTLA agonist antibody 2.8.6 to ameliorate a T cell driven model of colitis was assessed using the humanised mice. This T cell transfer model has previously been described as a murine model of inflammatory bowel disease (Ostanin et al., Am J Physiol Gastrointest Liver Physiol. 296:G135-46, 2009). CD45RB^hiCD25-CD4+ T cells sorted from spleens and lymph nodes of humanised BTLA mice were injected intraperitoneally into Rag1 KO recipients, (Rag1^tm1Mom; The Jackson Laboratory), at a dose of 5×10⁵cells per mouse. The transferred T cells cause an inflammatory colitis that develops after approximately 3 weeks and leads to diarrhea and weight loss. Rag1 KO cagemates that did not receive transferred T cells serve as non-diseased controls. On days 7, 21 and 35 after T cell transfer the recipient mice were injected intraperitoneally with 200 μg of 2.8.6 or isotype control antibody. All mice were weighed regularly, and at 8 weeks colons were weighed and measured and inflammatory infiltration assessed by histology, as well as by cell counting and flow cytometry of extracted lamina propria leucocytes. Antibody 2.8.6 prevented weight loss (FIG. 8a) and significantly reduced inflammatory infiltration of colons (FIG. 8b). Colon inflammation in diseased mice led to an increased colon weight:length ratio that was not seen in 2.8.6 treated mice (FIG. 8c).

US11421030B2. BTLA antibodies (2022-08-23). Oxford University Innovation Limited [GB], MiroBio Limited [GB]. Inventors: Simon John Davis [GB], Richard John Cornall [GB], Christopher Douglas Paluch [GB].

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Intestinal Inflammation Mouse Model

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The mouse lines p38αΔIEC (Mapk14^fl/fl-VilCre) and IEC-IKKβ^EE (transgenic Vil-IKKβ^EE) were previously described (8 (link), 12 (link)). RAG1-knockout mice (Rag1^tm1Mom) were obtained from the Jackson Laboratory. All mice were on a C57BL/6 background and maintained in a specific-pathogen-free condition. To suppress establishment of the intestinal microbiota, mice were administered a mixture of the following antibiotics in drinking water: ampicillin (1g/L), neomycin sulfate (1 g/L), vancomycin (0.5 g/L), and metronidazole (1g/L; all from Sigma). Treatment with antibiotics began in utero by providing antibiotics to the mothers as soon as the mating cages were set up, and continued postnatally until the mice were sacrificed for analysis. To induce colitis, mice were administered 2.5% or 3.5% dextran sulfate sodium (DSS) in drinking water for seven days; afterwards, drinking water without DSS was provided. Survival was monitored daily over a period of fourteen days. All animal experiments were conducted under Institutional Animal Care and Use Committee-approved protocols.

Caballero-Franco C., Guma M., Choo M.K., Sano Y., Enzler T., Karin M., Mizoguchi A, & Park J.M. (2016). Epithelial control of gut-associated lymphoid tissue formation through p38α-dependent restraint of NF-κB signaling. Journal of immunology (Baltimore, Md. : 1950), 196(5), 2368-2376.

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Generation and Characterization of X-MAID Mice

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Moesin knockout (MKO) mice on the C57BL/6 background were described previously (28 (link)–30 (link)). Mice homozygous for Rag1^tm1mom (RagKO) were obtained from Jackson Laboratories and bred in house. CRISPR mice in which the murine moesin gene was edited to contain the R171W mutation found in the majority of X-MAID patients (X-MAID mice) were generated by the CRISPR/Cas9 Mouse Targeting Core Facility, together with the Transgenic and Chimeric Mouse Facility at the University of Pennsylvania, following protocols published in (31 (link)). Briefly, Cas9 mRNA, gRNA, and ssDNA oligos containing the R171W X-MAID point mutation were designed and injected into C57BL/6J zygotes. Embryos were then transferred into pseudopregnant mice, creating the F0 chimeric generation. All founder mice were screened for chimerism and bred to determine germline transmission of the mutation. X-MAID mice were backcrossed to C57BL/6J mice (Jackson Laboratories) for at least 4 generations. Results from two independent founder lines were in agreement. All mice were bred in-house under SPF conditions and used at 3-5 weeks of age, all in accordance with protocols approved by the Institutional Animal Care and Use Committee of the Children’s Hospital of Philadelphia Research Institute. Exclusively male mice were used of every genotype, with WT mice being littermates to X-MAID mice.

Avery L., Robertson T.F., Wu C.F., Roy N.H., Chauvin S.D., Perkey E., Vanderbeck A., Maillard I, & Burkhardt J.K. (2022). A Murine Model of X-Linked Moesin-Associated Immunodeficiency (X-MAID) Reveals Defects in T Cell Homeostasis and Migration. Frontiers in Immunology, 12, 726406.

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Murine Transplant Experiments Protocol

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C57BL/6J and C57BL/6J Ly5.2-Cr (CD45.1) strains were obtained from The Jackson Laboratory (Bar Harbor, Maine) and used at 6–12 weeks of age. Balb/cJ, C57Bl/6-Tg(TcraTcrb)1100Mjb/J (OT-I), and RAG1^tm1Mom (RAG1 knockout) were obtained from The Jackson Laboratory and bred at Emory University or Johns Hopkins University. All transplant experiments were conducted in age-matched hosts randomly assigned to experimental groups. This study was conducted in accordance with the recommendations in the Guide for the Care and Use of Laboratory Animals. The protocol was approved by the Animal Care and Use Committee at Emory University and Johns Hopkins University. Animals were housed in specific pathogen-free animal facilities at Emory University and Johns Hopkins University.

Cohen G.S., Kallarakal M.A., Jayaraman S., Ibukun F.I., Tong K.P., Orzolek L.D., Benjamin Larman H, & Krummey S.M. (2023). Transplantation elicits a clonally diverse CD8+ T cell response that is comprised of potent CD43+ effectors. Cell reports, 42(8), 112993.

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Adoptive T Cell Transfer Colitis

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The adoptive T cell transfer colitis experiments were carried out as previously described^{77 (link)}. Briefly, T cells were isolated from the spleens of 8- to 12-week-old knockout and wild-type littermate mice by magnetic cell sorting using the Dynabeads Untouched Mouse CD4 cells kit according to the manufacturer's instructions (Life Technologies). Cells were then sorted on the BD FACS Aria II Cell Sorter (BD Biosciences) at 99% purity for CD4⁺CD25⁻CD45RB^hi cells, and 7.5 × 10⁵ cells were injected intraperitoneally into sex-matched RAG12M (Taconic) recipients for Dock2^−/−, Nckap1l^−/−, and wild-type littermate control mice and Rag1^tm1Mom (Jackson Laboratory) recipients for Gpsm3^−/−, Aif1^−/−, and wild-type littermate control mice. Mice were weighed weekly until clinical signs of disease were apparent. Antibodies to TCR-β (PerCP-Cy5.5) and CD4 (APC) were used in staining of splenocytes on the day of sacrifice to test for T cell engraftment, which ranged from 3–15% for all mice except Dock2^−/− mice. Mouse intestine was evaluated at sacrifice for gross anatomical signs of disease.

Peters L.A., Perrigoue J., Mortha A., Iuga A., Song W.M., Neiman E.M., Llewellyn S.R., Di Narzo A., Kidd B.A., Telesco S.E., Zhao Y., Stojmirovic A., Sendecki J., Shameer K., Miotto R., Losic B., Shah H., Lee E., Wang M., Faith J.J., Kasarskis A., Brodmerkel C., Curran M., Das A., Friedman J.R., Fukui Y., Humphrey M.B., Iritani B.M., Sibinga N., Tarrant T.K., Argmann C., Hao K., Roussos P., Zhu J., Zhang B., Dobrin R., Mayer L.F, & Schadt E.E. (2017). A functional genomics predictive network model identifies regulators of inflammatory bowel disease. Nature genetics, 49(10), 1437-1449.

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Mouse Strains for Immunological Studies

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Inbred C57/Bl6J and Rag1-deficient Mice

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Inbred wildtype (WT) C57/Bl6J mice were obtained from Charles River (Sulzfeld, Germany) and housed under conventional conditions at the animal facilities of the Research Institute for Experimental Medicine (FEM, Charité - Universitätsmedizin Berlin). Recombination activating gene 1-deficient mice (Rag^1tm1Mom) on a C57BL/6 background were purchased from Jackson Laboratory (Bar Harbor, United States) and bred under SPF conditions at the FEM. All animals were kept in polycarbonate cages and had free access to sterile standard chow and drinking water. All experiments were performed in accordance with the German legislation on the protection of animals and approved by the local authorities (Landesamt für Gesundheit und Soziales, registration number G0422/17).

Golusda L., Kühl A.A., Lehmann M., Dahlke K., Mueller S., Boehm-Sturm P., Saatz J., Traub H., Schnorr J., Freise C., Taupitz M., Biskup K., Blanchard V., Klein O., Sack I., Siegmund B, & Paclik D. (2022). Visualization of Inflammation in Experimental Colitis by Magnetic Resonance Imaging Using Very Small Superparamagnetic Iron Oxide Particles. Frontiers in Physiology, 13, 862212.

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