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Nod ltj

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The NOD/LtJ is a laboratory mouse strain used in research. It is a non-obese diabetic (NOD) mouse model that develops autoimmune diabetes spontaneously. The strain is maintained on the LtJ background.

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C57bl 6j, by Jackson ImmunoResearch (5 mentions) C57bl 6, by Jackson ImmunoResearch (4 mentions) C3h hej, by Jackson ImmunoResearch (3 mentions) 129s1 svimj, by Jackson ImmunoResearch (3 mentions) Balb cj, by Jackson ImmunoResearch (3 mentions) Cba j, by Jackson ImmunoResearch (2 mentions) Akr j, by Jackson ImmunoResearch (2 mentions) Sjl j, by Jackson ImmunoResearch (2 mentions) Dba 2j, by Jackson ImmunoResearch (2 mentions) Pwk phj, by Jackson ImmunoResearch (2 mentions) Nzw lacj, by Jackson ImmunoResearch (2 mentions) Fvb nj, by Jackson ImmunoResearch (2 mentions) Rag1 b6.129s7 rag1tm1mom j, by Jackson ImmunoResearch (2 mentions) C3h hen, by Jackson ImmunoResearch (2 mentions) Thy1.1 nod, by Jackson ImmunoResearch (2 mentions) Nod scid, by Jackson ImmunoResearch (2 mentions) Ascensia microfill blood glucose test strips, by Bayer (2 mentions) Ot 2 tcr tg, by Jackson ImmunoResearch (2 mentions) Wild type c57bl 6, by Jackson ImmunoResearch (1 mentions) Nod ltj mice, by Jackson ImmunoResearch (1 mentions)

17 protocols using nod ltj

1

Generating Lineage-Tracing NOD Mouse Model

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Wild-type C57BL/6, NOD/LtJ, and R26EGFP NOD were purchased from the Jackson Laboratory. SJL/J and congenic H-2g7 C57BL/6 were purchased from National Cancer Institute animal production program. The RIPCreERT mice were obtained from the Melton laboratory at Harvard University (18 ). Sox9CreERT mice were previously described (73 (link)) and provided by M. Sander’s laboratory at University of California San Diego. GlurtTATetOCreR26tdRFP mice were provided by P.S.’s laboratory at University of Calgary. NesCreERT NOD mice were backcrossed from NesCreERT B6 mice purchased from Jackson Laboratory. Lineage-tracing NOD mice were generated by crossing two strains of NOD mice at City of Hope Animal Research Facilities (COH ARC). Breeding strategies are described in SI Appendix. All experimental mice were housed in the specific pathogen-free rooms in the ARC. The animal use procedures were approved by the COH Institutional Animal Care and Use Committee.
Tang S., Zhang M., Zeng S., Huang Y., Qin M., Nasri U., Santamaria P., Riggs A.D., Jin L, & Zeng D. (2020). Reversal of autoimmunity by mixed chimerism enables reactivation of β cells and transdifferentiation of α cells in diabetic NOD mice. Proceedings of the National Academy of Sciences of the United States of America, 117(49), 31219-31230.
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2

Diabetes Development in NOD Mouse Models

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NOD/LtJ mice purchased from the Jackson Laboratory were used for studying diabetes development. NOD/Caj mice were originally obtained from the Jackson Laboratory (NOD/LtJ) and have been maintained at Yale University for over 25 years. MyD88−/−NOD mice were generated as described previously [20 (link)] and have been maintained at Yale University for over 7 years. MyD88−/−B6 mice were kindly provided by Dr. Akira [21 (link)] and have been maintained at Yale University for over 10 years. B6g7 breeders were kindly provided by Drs. Mathis and Benoist (Harvard University) and have been bred at Yale University for over 10 years. MyD88−/−B6g7 mice were generated by breeding B6g7 with MyD88−/−B6 mice. C57BL/6J (B6) mice were originally obtained form the Jackson Laboratory and have been maintained at Yale University for over 5 years. All mice used in this study were kept in the same room, in specific pathogen–free conditions, in a 12-hour dark/light cycle and housed in individually-ventilated filter cages with autoclaved food at the Yale University animal facility. The use of the animals in this study was approved by the Yale University Institutional Animal Care and Use Committee.
Peng J., Narasimhan S., Marchesi J.R., Benson A., Wong F.S, & Wen L. (2014). Long Term Effect of Gut Microbiota Transfer on Diabetes Development. Journal of autoimmunity, 53, 85-94.
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3

Glycemic Monitoring in NOD/LtJ Mice

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NOD/LtJ were originally obtained from Jackson laboratory Care and handling of mice followed Institutional Animal Care and Use Committee rules. Glycemia of all animals was measured weekly from a drop of blood collected from the tip of the tail.
Bernstein H.D, & Hyndman J.B. (2001). Physiological Basis for Conservation of the Signal Recognition Particle Targeting Pathway in Escherichia coli. Journal of Bacteriology, 183(7), 2187-2197.
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4

Mouse Diversity Panel Protocol

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Thirty-six male inbred mouse strains (129S1/SvImJ, 129X1/SvJ, A/J, AKR/J, BALB/cByJ, BTBR T+Itpr3tf/J, BUB/BnJ, C3H/HeJ, C57BLKS/J, C57BL/6J, C57BR/cdJ, C58/J, CBA/J, CZECHII/EiJ, DBA/2J, FVB/NJ, I/LnJ, KK/HiJ, LG/J, LP/J, MA/MyJ, NOD/LtJ, NON/LtJ, NZB/BINJ, NZO/HiLtJ, NZW/LacJ, PERA/EiJ, PL/J, PWD/PhJ, PWK/PhJ, RIIIS/J, SEA/GnJ, SJL/J, SM/J, SWR/J, and WSB/EiJ), aged 10–12 weeks, were obtained from The Jackson Laboratory (Bar Harbor, ME, USA). This panel of isogenic mice was chosen based on priority strains from the Mouse Diversity Panel.26 (link) Four mice were used per strain. Male mice were housed four per cage in polycarbonate cages on a 12-hour light/dark cycle (lights on at 7 am), with access to food and water ad libitum. All procedures were approved by the Institutional Animal Care and Use Committee and followed the guidelines set forth by the National Institutes of Health (NIH) Guide for the Care and Use of Laboratory Animals.
Frick A., Fedoriw Y., Richards K., Damania B., Parks B., Suzuki O., Benton C.S., Chan E., Thomas R.S, & Wiltshire T. (2015). Immune cell-based screening assay for response to anticancer agents: applications in pharmacogenomics. Pharmacogenomics and Personalized Medicine, 8, 81-98.
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5

Comprehensive Mouse Cohort Characterization

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BALB/cJ, C57BL/6J, NOD/LtJ, C3H/HeN, RAG1−/− (B6.129S7-Rag1tm1Mom/J), Fut2−/− (B6.129X1-Fut2tm1Sdo/J), Villin-cre (B6.SJL-Tg(Vil-cre)997Gum/J), and CD11c-cre (C57BL/6J-Tg(Itgax-cre,-EGFP)4097Ach/J) mice were purchased from The Jackson Laboratory (Bar Harbor, ME). Fut2−/− mice were backcrossed greater than 7 generations to BALB/c. Knock-out mice produced litters of mixed genotypes kept cohoused to homogenize their gut microbiota. B6 MyD88−/− mice were a generous gift of Shizuo Akira (Osaka University). B6 MyD88 floxed mice were described 31 (link). Rorc−/−32 (link), and IL-23p19−/−33 (link) were provided by Yang-Xin Fu (The University of Chicago). IL-22−/− mice 34 (link) were maintained at the Memorial Sloan-Kettering Cancer Center. Mice were housed in a specific pathogen-free facility and used in accordance with institutional guidelines for animal welfare. 6-12 week old male and female mice were used for randomization purposes. The numbers of mice per group were chosen as the minimum needed to obtain biologically significant results, based on previous experience. Evaluations were made in a blind fashion. Functional experiments were done with Fut2-negative mice on the BALB/c genetic background using Fut2-sufficient littermates as controls.
Pickard J.M., Maurice C.F., Kinnebrew M.A., Abt M.C., Schenten D., Golovkina T., Bogatyrev S.R., Ismagilov R.F., Pamer E.G., Turnbaugh P.J, & Chervonsky A.V. (2014). Rapid fucosylation of intestinal epithelium sustains host-commensal symbiosis in sickness. Nature, 514(7524), 638-641.
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6

NOD Mouse Strain Handling Protocol

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NOD.CD28-/- mice (41 (link), 51 (link)) were kindly provided by Dr. Tang (UCSF, San Francisco, CA, USA). NOD/LtJ, Thy1.1 NOD, FoxP3GFP.NOD, and NSG (NOD scid gamma) mice were purchased from Jackson Laboratories (Bar Harbor, ME). All mice were bred and maintained under specific pathogen-free conditions, with 12-hour light/dark cycles and food and water ad libitum, in accordance with protocols approved by the Indiana University Animal Care and Use Committee.
Obarorakpor N., Patel D., Boyarov R., Amarsaikhan N., Cepeda J.R., Eastes D., Robertson S., Johnson T., Yang K., Tang Q, & Zhang L. (2023). Regulatory T cells targeting a pathogenic MHC class II: Insulin peptide epitope postpone spontaneous autoimmune diabetes. Frontiers in Immunology, 14, 1207108.
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7

Comprehensive Mouse Cohort Characterization

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BALB/cJ, C57BL/6J, NOD/LtJ, C3H/HeN, RAG1−/− (B6.129S7-Rag1tm1Mom/J), Fut2−/− (B6.129X1-Fut2tm1Sdo/J), Villin-cre (B6.SJL-Tg(Vil-cre)997Gum/J), and CD11c-cre (C57BL/6J-Tg(Itgax-cre,-EGFP)4097Ach/J) mice were purchased from The Jackson Laboratory (Bar Harbor, ME). Fut2−/− mice were backcrossed greater than 7 generations to BALB/c. Knock-out mice produced litters of mixed genotypes kept cohoused to homogenize their gut microbiota. B6 MyD88−/− mice were a generous gift of Shizuo Akira (Osaka University). B6 MyD88 floxed mice were described 31 (link). Rorc−/−32 (link), and IL-23p19−/−33 (link) were provided by Yang-Xin Fu (The University of Chicago). IL-22−/− mice 34 (link) were maintained at the Memorial Sloan-Kettering Cancer Center. Mice were housed in a specific pathogen-free facility and used in accordance with institutional guidelines for animal welfare. 6-12 week old male and female mice were used for randomization purposes. The numbers of mice per group were chosen as the minimum needed to obtain biologically significant results, based on previous experience. Evaluations were made in a blind fashion. Functional experiments were done with Fut2-negative mice on the BALB/c genetic background using Fut2-sufficient littermates as controls.
Pickard J.M., Maurice C.F., Kinnebrew M.A., Abt M.C., Schenten D., Golovkina T., Bogatyrev S.R., Ismagilov R.F., Pamer E.G., Turnbaugh P.J, & Chervonsky A.V. (2014). Rapid fucosylation of intestinal epithelium sustains host-commensal symbiosis in sickness. Nature, 514(7524), 638-641.
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8

Murine Type 1 Diabetes Prevention

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Male and female NODLt/J and C57BL/6J mice between the ages of 2 and 10 weeks were purchased from the Jackson Laboratories (Bar Harbor, ME, USA) and maintained in a specific pathogen-free environment at the Animal Research Facility of the Allegheny Health Network. All mice were 2 weeks of age upon arrival at our facility. Where the effect of study agents (MPO/neutrophil elastase inhibitors) on diabetes incidence was the primary outcome measure in T1D diabetes prevention, mice were randomized into the treatment arms and study agents were administered thereafter, initiated at 3 weeks of age. All experiments and animal euthanasia were conducted in line with specific protocols approved by the Allegheny Health Network IACUC.
Garciafigueroa Y., Phillips B.E., Engman C., Trucco M, & Giannoukakis N. (2021). Neutrophil-Associated Inflammatory Changes in the Pre-Diabetic Pancreas of Early-Age NOD Mice. Frontiers in Endocrinology, 12, 565981.
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9

Generation of Ica1 Knockout Mouse Models

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All animal protocols were reviewed and approved by the University of Pittsburgh Institutional Animal Care and Use Committee. NOD/Ltj and C57BL/6 mice were purchased from the Jackson Laboratory (Bar Harbor, ME). Only female NOD/Ltj mice were used in the study. Mice with two loxp sites genetically engineered to flank exon 14 of the Ica1 gene (floxed) were generated through standard gene targeting methods as previously described [24 (link),30 (link)]. Detailed procedures for assembling the Ica1 exon 14 targeting construct used in the study are available upon request. Heterozygous ICAflox/wt mice were backcrossed to C57BL/6 mice for five generations before intercross to obtain the homozygous ICAflox/flox. To generate the Aire-ΔICA69 line, ICAflox/flox mice were crossed to the Aire-Cre transgenic mice [24 (link)], developed in our laboratory. To generate the ICAdel/wt line, ICAflox/wt mice were first crossed to B6.CMV–Cre transgenic mice to obtain the Ica1del allele in the germline, followed by further backcrossing to C57BL/6 mice to breed out the CMV-Cre transgene (Jackson Laboratory). Of note, all the Ica1 genetically modified mouse lines used in this study (i.e., ICAdel/wt, ICAflox/flox and Aire-ΔICA69) are on the B6 genetic background.
Fan Y., Gualtierotti G., Tajima A., Grupillo M., Coppola A., He J., Bertera S., Owens G., Pietropaolo M., Rudert W.A, & Trucco M. (2014). Compromised central tolerance of ICA69 induces multiple organ autoimmunity. Journal of autoimmunity, 53, 10-25.
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10

Immunization of NOD/LtJ Mice with PRPH

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NOD/LtJ and NOR mice were obtained from The Jackson Laboratory (Bar Harbor, Maine, USA) and further bred in our specific pathogen-free animal facilities. C57BL/6 mice were obtained from Charles River Laboratories (Spain).
To test the humoral or cellular B cell response to PRPH, NOD/LtJ were immunized i.p. or s.c. at 6-12 weeks of age with 100 μg of recombinant PRPH429-507 emulsified in complete Freund's adjuvant (CFA, Sigma) or CFA only as a control.
Garabatos N., Alvarez R., Carrillo J., Carrascal J., Izquierdo C., Chapman H.D., Presa M., Mora C., Serreze D.V., Verdaguer J, & Stratmann T. (2014). In vivo detection of peripherin-specific autoreactive B cells during type 1 diabetes pathogenesis. Journal of immunology (Baltimore, Md. : 1950), 192(7), 3080-3090.
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