Search Criteria: Research Area is "Diabetes and Obesity Research: Type 1 Diabetes (IDDM) Analysis Strains"
Strains from the Research Colonies of Jackson Laboratory Scientists
New Strains Under Development
| Stock Number |
Strain Name Phenotype |
Standard Supply |
| 001303 | NOD.CB17-Prkdcscid/J | Level 1 |
| Mice homozygous for the severe combined immune deficiency spontaneous mutation (Prkdcscid, commonly referred to as scid) are characterized by an absence of functional T cells and B cells, lymphopenia, hypogammaglobulinemia, and a normal hematopoietic microenvironment. Normal antigen-presenting cell, myeloid, and NK cell functions are strain dependent. scid mice carry a DNA repair defect and a defect in the rearrangement of genes that code for antigen-specific receptors on lymphocytes. Most homozygotes have no detectable IgM, IgG1, IgG2a, IgG2b, IgG3, or IgA. Thymus, lymph nodes, and splenic follicles are virtually devoid of lymphocytes. scid mice accept allogeneic and xenogeneic grafts making them an ideal model for cell transfer experiments. Some scid mice will spontaneously develop partial immune reactivity. scid mice that have serum Ig levels greater than 1 ug/ml are considered "leaky." scid leakiness is highly strain depen
..... For more information please see the full phenotype on the strain data sheet | ||
| 000686 | SJL/J | Level 2 |
| SJL mice display a very high incidence of reticulum cell sarcomas resembling Hodgkin's disease by approximately one year of age. Sarcomas first appear in the Peyer's patches and mesenteric lymph nodes and later in the spleen, liver, thymus and other lymph nodes. Most of the tumors are mixed-cell types classified as type B reticulum cell neoplasms, but a few are type A histiocytomas. This strain is also characterized by extreme aggression in males and its susceptibility to experimental autoimmune encephalomyelitis (EAE) for multiple sclerosis research. SJL/J mice develop a spontaneous myopathy resulting from a splice-site mutation in the Dysferlin gene. This Dysfim allele has been shown to result in decreased levels of dysferlin protein in SJL/J mice and makes this strain a good model for limb girdle muscular dystrophy 2B. This spontaneous myopathy is characterized by a progressive loss of muscle mass and strength corresponding with an increase in muscle pathology incl
..... For more information please see the full phenotype on the strain data sheet | ||
| 000689 | SWR/J | Level 3 |
| SWR/J mice are used widely in research as a general purpose strain. Aging mice exhibit a high incidence of lung and mammary gland tumors. They also develop extreme polydipsia and polyuria (nephrogenic diabetes insipidus) with increasing age. SWR/J mice are highly susceptible to experimental allergic encephalomyelitis (EAE). Germline deletion of about 50% of T-cell receptor V beta-chain gene segments and a T-cell receptor V alpha polymorphism are responsible for the resistance of SWR/J mice to collagen type II-induced arthritis. SWR/J mice show an intermediate susceptibility to developing atherosclerotic aortic lesions (1670 to 1690 um2 atherosclerotic aortic lesions/aortic cross-section) following 14 weeks on an atherogenic diet (1.25% cholesterol, 0.5% cholic acid and 15% fat). SWR/J mice have been recommended for generation and propogation of transgenic mice because they are high responders to exogenous hormones, have large and prominant pronuclei with good resistance to l
..... For more information please see the full phenotype on the strain data sheet | ||
| 002570 | NOD.Cg-Prkdcscid B2mtm1Unc/J | Level 4 |
| Mice homozygous for both the B2mtm1Unc and Prkdcscid (commonly referred to as scid) mutations on the NOD/ShiLtSz background are class I deficient, B and T cell deficient, C-5 deficient (Hc0), and have low NK cells. This strain is an ideal model for xenograft transplantation studies and is an excellent source for insulitis-free, MHC class I-negative islets for transplantation studies. | ||
| 002050 | NOR/LtJ | Level 4 |
| NOR/LtJ mice are insulitis resistant and diabetes free. NOR/LtJ mice still exhibit peripheral T-lymphocyte accumulation and defective peritoneal macrophage responses characteristic of NOD/LtJ mice. NOR/LtJ mice are matched at the diabetogenic H2g7 complex to NOD/LtJ. | ||
| 006500 | 129.NOD-(D17Mit175-H2)/J | Repository- Live |
| 129S1.NOD-H2g7 congenic mice are viable, fertile, normal in size, do not display any gross physical or behavioral abnormalities and are diabetes free. Because targeted mutations frequently are made using 129 ES cells, this strain may be useful for identifying Idds in 129 strains. | ||
| 003070 | ALR/LtJ | Repository- Live |
| ALS/LtJ (Stock No. 003072) and ALR/LtJ inbred strains are of interest to investigators across a wide range of scientific disciplines including type 1 and type 2 diabetes, obesity, metabolism and toxicology research. Treatment of alloxan or streptozotocin causing pancreatic beta cell destruction, leads to severe hyperglycemia and hypoinsulinemia in ALS/LtJ mice. ALR/LtJ mice are resistant to these toxins. ALR/LtJ mice are of particular interest to investigators studying the immunogenetics of NOD/LtJ mice in that the ALR/LtJ MHC haplotype (H2gx) is a variant of the diabetogenic NOD H2g7 haplotype. The (H2gx) haplotype is identical to the H2g7 haplotype from the H2-K end of the complex through the class II and class III region distal to Hsp70. However, at the distal H2-D end of the complex, ALR/LtJ mice have a rare H2-Dgx allele. Despite the similarities to the NOD/ShiLtJ mice, ALR/LtJ mice do not develop
..... For more information please see the full phenotype on the strain data sheet | ||
| 003072 | ALS/LtJ | Repository- Live |
| ALS/LtJ and ALR/LtJ (Stock No. 003070) inbred strains are of interest to investigators across a wide range of scientific disciplines including type 1 and type 2 diabetes, obesity, metabolism and toxicology research. Treatment of alloxan or streptozotocin causing pancreatic beta cell destruction, leads to severe hyperglycemia and hypoinsulinemia in ALS/LtJ mice. ALR/LtJ mice are resistant to these toxins. By 34 wk of age, both untreated ALS/Lt and ALR/Lt males fed a 6% fat-containing chow diet attain a mean body weight of around 50 grams. Genome wide scan comparison shows that ALS/LtJ mice are more closely related to NON/ShiLtJ mice (they share the H2nb1 haplotype) than to NOD/ShiLtJ. Like two other ICR-derived inbred strains selected in Japan (NON and NSY), alloxan-untreated ALS/Lt males exhibit impaired glucose tolerance when tested by intraperitoneal administration of glucose. However, unlike NON/ShiLt males, which exhibit impaired glucose tolerance in the presence
..... For more information please see the full phenotype on the strain data sheet | ||
| 006411 | B6.129-Gasttm1(INS)Ez/J | Repository- Live |
| Mice heterozygous for this "G-InsKi" allele are viable and fertile. Human insulin expressed from this mutant allele retains full biological activity. Expression of human insulin is specific to gastrin-expressing cells (G cells of the antral stomach and some duodenum cells), and is released into portal circulation in response to the same meal-associated stimuli that control gastrin release. Heterozygous mice exhibit normal blood glucose levels, and toxic hypoglycemia is not observed. The donating investigators report that human insulin levels are sufficient to activate insulin signaling cascades in the liver but not in skeletal muscle. These mutant mice may be useful for diabetes and obesity research, specifically for studying the molecular and physiological mechanisms by which the hepatic action of transgenic insulin prolongs the survival of diabetic mice (e.g. Ins2Akita mutant mice). | ||
| 006860 | B6.129-Ins2Akita Bdkrb2tm1Jfh/SmiJ | Repository- Live |
| Mice homozygous for the targeted mutation and heterozygous for the Akita spontaneous mutation are viable and fertile. Similar to mice only heterozygous for the Akita mutation, the double mutant mice are severely diabetic: their body weights are 70% of wildtype, they consume over 3-fold the normal amount of food, and their urinary output is approximately 20-fold more than that of wildtype mice. Double mutant mice have markedly enlarged kidneys. Urinary albumin excretion in double mutants is almost 4-fold that of either single mutant, and double mutants experience more severe nephropathy than mice that are heterozygous for the Akita mutation alone. Megsin and nephrin expression is markedly increased in double mutant mice when compared to wildtype or to mice with either single mutation alone. By 12 months of age, double mutant mice experience hair loss due to a reduction in hair follicle numbers and thinning of the dermis. Double mutants have essentially no subcutaneo
..... For more information please see the full phenotype on the strain data sheet | ||
| 006580 | B6.Cg-Ins2Akita Ldlrtm1Her/J | Repository- Live |
| Mice homozygous for the Akita spontaneous mutation die postnatally, typically by 12 weeks of age. Independently, heterozygous Akita mutant mice are a model of insulin dependent diabetes mellitus (IDDM) with severe hyperglycemia (see the datasheet for Stock No. 003548 for additional information). LDLR-null homozygotes have elevated serum cholesterol levels (200-400 mg/dl) which can escalate to very high levels (> 2000 mg/dl) when the mice are fed a high fat diet. LDLR-deficient mice also are predisposed to develop atherosclerosis. These double mutant mice may be useful in studies of diabetes, metabolism, hyperglycemia, atherosclerosis, hypercholesterolemia, and diabetes-related macrovascular complications. | ||
| 004369 | B6.Cg-Rag1tm1Mom Ins2Akita/J | Repository- Live |
| Mice homozygous for the Rag1 targeted mutation and heterozygous for the Akita spontaneous display the diabetes phenotype in the absence of B and T cells and unlike single Akita mice, double mutants do not reject allografts. Mice heterozygous for only the Akita spontaneous mutation are viable and fertile. (Homozygotes typically die by 12 weeks of age from extreme hyperglycemia.) Symptoms in heterozygous mutant mice include hyperglycemia, hypoinsulinemia, polydipsia, and polyuria, beginning at approximately 3-4 weeks of age. The diabetic phenotype is more severe and progressive in heterozygous males than in females. Obesity and insulitis do not accompany diabetes. This double mutant strain is ideally suited for use in allogeneic or xenogeneic islet or stem cell transplantation protocols because the mice are severely immunocompromised and spontaneously develop diabetes at a young age. | ||
| 006872 | B6.Cg-Tg(Ins1-DsRed*T4)32Hara/J | Repository- Live |
| Mice hemizygous for this "MIP-RFP" transgene are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. These transgenic mice express the DsRed.T4 variant of Enhanced Red Fluorescent Protein under the control of mouse insulin 1 promoter. Fluorescence is detected in tissues where insulin I is normally expressed; fluorescent protein expression in pancreatic beta-cells is evident from embryonic day (E)13.5 through adult. Transgenic mice exhibit normal glucose tolerance and pancreatic insulin levels. While the human growth hormone sequence in the transgene is designed to enhance expression of the fluorescent protein and is not expressed in a similarly constructed transgene (see Stock No. 006864), whether or not it is expressed for this strain was not characterized. This mutant mouse strain may be useful in studies of pancreatic development and pancreatic beta islet cell biology. In an a
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| 006864 | B6.Cg-Tg(Ins1-EGFP)1Hara/J | Repository- Live |
| Mice hemizygous for this "MIP-GFP" transgene are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. These transgenic mice express Enhanced Green Fluorescent Protein (EGFP) under the control of the mouse insulin 1 promoter. Fluorescence is detected in tissues where insulin I is normally expressed; fluorescent protein expression in pancreatic beta-cells is evident from embryonic day (E)13.5 through adulthood. The fluorescence expression pattern is similar to the patterns seen in other stocks (see Stock No. 006784 and Stock No. 006866). MIP-GFP transgenic mice exhibit normal glucose tolerance and pancreatic insulin levels. The human growth hormone (hGH) sequence in the transgenic insert enhances expression of the EGFP, but hGH is not expressed. This mutant mouse strain may be useful in studies of diabetes and pancreatic beta islet
..... For more information please see the full phenotype on the strain data sheet | ||
| 003548 | C57BL/6-Ins2Akita/J | Repository- Live |
| Mice heterozygous for the Akita spontaneous mutation (Ins2Akita) are viable and fertile. Symptoms in heterozygous mutant mice include hyperglycemia, hypoinsulinemia, polydipsia, and polyuria, beginning around 3-4 weeks of age. The diabetic phenotype is more severe and progressive in the male than in the female. Obesity or insulitis does not accompany diabetes. Aged mice exhibit gait disturbance and decreased sensory nerve conduction velocity, but do not exhibit learning or memory deficits (Choeiri C et al., 2005). Progressive retinal abnormalities begin as early as 12 weeks after the onset of hyperglycemia. Retinal complications include increased vascular permeability, alterations in the morphology of astrocytes and microglia, increased apoptosis and thining of the inner layers of the retina. (Barber AJ, et al., 2005) The mean lifespan of diabetic male mice on the C57BL/NJcl background (305 days) was significantly shorter than that of nondiabetic males in anothe
..... For more information please see the full phenotype on the strain data sheet | ||
| 007562 | D2.B6-Ins2Akita/MatbJ | Repository- Live |
| DBA/2J mice heterozygous for the Akita spontaneous mutation are viable and fertile. The donating investigator reports that the symptoms in heterozygous mutant mice are more severe and progressive in the males than in the females and include hyperglycemia, hypoinsulinemia, polydipsia, and polyuria, beginning at approximately 3-4 weeks of age. Obesity and insulitis do not accompany diabetes. Litter sizes range from 2-8 pups. Heterozygous Akita males develop albuminuria at two months of age. The albuminuria is progressive such that by 6 months of age albumin/creatine levels are approximately 600ug/mg. Additionally, it has been reported that DBA/2J heterozygous mutant mice develop diabetic nephropathy.
Although not studied in the DBA/2J heterozygotes, C57BL/6 heterozygous mutant mice exhibit gait disturbance and decreased sensory nerve conduction velocity, but do not exhibit learning or memory deficits (Choeiri C et al., 2005). Progressive retinal abnormalities begin as early as
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| 005564 | FVB(Cg)-Tg(Ins2-CALM1)26Ove Tg(Cryaa-TAg)1Ove/PneJ | Repository- Live |
| Transgenic mice are viable, display small eyes with cataracts and are hyperglycemic within 24 hours of age. S1 Nuclease protection assays indicate expression of calmodulin in the pancreas of 40-60 day old transgenic mice. Immunofluorescence analysis of the pancreas indicates increased levels of camodulin in B-cells of the pancreas. Camodulin fluorescing cells were not detected in the pancreatic acinar cells or any other tissue. Digital image scanning indicates the concentration of camodulin in transgenic B-cells is 5-fold higher than in wild type controls. Pancreatic insulin is 28% of control levels by 15 days of age. Insulin mRNA levels were also reduced in the transgenic animals. Transgenic mice experience hypoalbuminemia, elevated blood pressure, impaired cardiomyocytes and late stage diabetic nephropathy. Although transgenic mice are hyperglycemic within 24 hours of age, they are able to survive over a year without insulin treatment. This stock is useful for studying systemic c
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| 006867 | FVB.B6-Ins2Akita/MlnJ | Repository- Live |
| FVB/NJ mice heterozygous for the Akita spontaneous mutation are viable and fertile. The donating investigator reports that the symptoms in heterozygous mutant mice are more severe than those observed in C57BL/6-Ins2Akita mice (Stock No. 003548). These symptoms include hyperglycemia (females > 600mg/dl, males ~560 mg/dl), hypoinsulinemia, polydipsia, and polyuria, beginning at approximately 3-4 weeks of age. In contrast to Akita heterozygotes on a C57BL/6 background, FVB/NJ adult heterozygous females are more hyperglycemic than heterozygous males. Obesity and insulitis do not accompany diabetes. Ins2 is expressed in the fetal yolk sac and is maternally imprinted. Heterozygous mutant females become more hyperglycemic during pregnancy, and are susceptible to embryo malformations leading to reabsorption, even with insulin therapy. Heterozygous mutant males do not produce mutant and wild-type offs
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..... For more information please see the full phenotype on the strain data sheet | ||
| 008063 | NOD-Chr 17NZM2328/McdfJ | Repository- Live |
| This NOD consomic strain, commonly referred to as NOD.Zc17 carries Chromosome 17 alleles, D17Mit164 (38Mb) through D17Mit73 (79Mb) derived from NZM2328. Diabetes incidence in this diabetes/lupus resistant strain is reported to be 0 in both females and males compared to 70% in female and 40% in male NOD/Bdc control mice. This strain will be useful to identify candidate genes associated with diabetes resistance and to identify genes with common roots in multiple autoimmune diseases. | ||
| 008062 | NOD-Chr 1NZM2328/McdfJ | Repository- Live |
| This NOD consomic strain, commonly referred to as NOD.Zc1, carries Chromosome 1 alleles, D1Mit316 (10Mb) through D1Mit293 (194Mb) derived from NZM2328 that includes the Idd5 region. NOD.Zc1 is viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. Diabetes incidence in this diabetes/lupus resistant strain is reported to be 10% in the females and 0% in males compared to 70% in female and 40% in male NOD/Bdc control mice. This strain will be useful to identify candidate genes associated with diabetes resistance and to identify genes with common roots in multiple autoimmune diseases. | ||
| 008064 | NOD-Chr 4NZM2328/McdfJ | Repository- Live |
| This NOD consomic strain, commonly referred to as NOD.Zc4 carries Chromosome 4 alleles, D4Mit18 (13Mb) through D4Mit59 (154Mb) derived from NZM2328. Diabetes incidence in this diabetes/lupus resistant strain is reported to be 7% in females and 0 for males compared to 70% in female and 40% in male NOD/Bdc control mice. This strain is useful for identifying candidate genes associated with diabetes resistance and to identify genes with common roots in multiple autoimmune diseases. | ||
| 006611 | NOD.129P2(B6)-B2mtm1Unc Tg(HLA-A/H2-D/B2M)1Dvs/DvsJ | Repository- Live |
| NOD mice carrying only the HLA-A/H2-D/B2M transgene, commonly referred to as NOD.HHD, (Stock No. 006604) develop significantly accelerated diabetes onset compared to NOD/ShiLtDvs (NOD) inbred mice.
This mutant stock is also homozygous for the B2mtm1Unc mutation which normally prevents the development of of CD8+ T cells. The presence of the transgene in the B2m-deficient background, however, restores CD8+ T cells, but at a significantly lower level than in NOD inbred mice. Due to the covalently linked nature of the B2M component encoded into the transgene, the transgenic construct is unable to rescue murine MHC class 1 molecules in the NOD.B2m deficient (Stock No. 002309) mice. Thus, these double mutant mice only express human HLA-A2.1. Fifty-five percent of these NOD transgenic B2m-deficient mice develop diabetes b
..... For more information please see the full phenotype on the strain data sheet | ||
| 005036 | NOD.129S2(B6)-Ins2tm1Jja/GseJ | Repository- Live |
| Ins2tm1Jja heterozygous mice are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. RT-PCR detects no expression of Ins2 in the thymus or pancreas of Ins2tm1Jja homozygous mice and Insulin Autoantibody Assays (IAA) indicate that by four weeks of age insulin auto-antibodies were significantly higher than NOD controls. Diabetes incidence occurs in 100 percent of the homozygous females by 15 weeks of age compared with 77% wildtype females by 27 weeks of age. While 100 percent of the homozygote males are diabetic by 22 weeks old compared to 28 percent of the wildtype males by 27 weeks of age. Histological evaluation found extensive islet infiltration in 8 week old homozygous mice compared to wildtype mice in which a minority of islets were infiltrated. NOD.129S2(B6)-Ins2tm1Jja/GseJ is useful for studying insulin autoantigens and their role in the autoimmune process leading
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| 003729 | NOD.129S7(B6)-Rag1tm1Mom/J | Repository- Live |
| Mice homozygous for the Rag1tm1Mom mutation produce no mature T cells or B cells. Their phenotype can be described as a "non-leaky" severe combined immune deficiency. (Prkdcscid/Prkdcscid) mice produce some B cells and IgM. NOD.129S7(B6)-Rag1tm1Mom/J mice have no CD3+ or T cell receptor (TCR) alpha-beta positive cells. The thymus of the mutant mice is severely involuted. The thymocytes are CD8-CD4- and most are IL2 receptor positive. Neither the spleen nor bone marrow contain any IgM or IgD staining cells, indicating an absence of mature B cells. These and other data suggest that both B cell and T cell development have been arrested at an early stage. Macroscopically, the mutants are indistinguishable from heterozygotes or normal wildtype siblings. Notable differences between this strain and the NOD.CB17-Prkdcscid/J strain (Stock No. 001303) include a longer life s
..... For more information please see the full phenotype on the strain data sheet | ||
| 007931 | NOD.A-Idd3A/J/MrkJ | Repository- Live |
| This NOD congenic strain, commonly referred to as NOD.A/J-Idd3, is carrying Chr 3 alleles, SNPS rs168642 (18.178Mb) through rs13477164, (66.638Mb) derived from strain A/J including the insulin dependent diabetes susceptibility 3 loci (Idd3). Diabetes onset and incidence among mice of this strain is reported to be similar to NOD/MrkTac, with approximately 65% of the females becoming diabetic by 200 days of age. The congenic NOD.A/J-Idd3 females are predisposed to autoimmune ovarian dysgenesis. Thymocytes and splenocytes, either non-activated or activated of this T1D susceptible stock produce less Il2 mRNA than T1D protected strains (Stock No's. 007933 and 007934). Il2 molecules derived from the A/J strain are identical to NOD. This congenic strain, one of a set of 5 strains (007930, For more information please see the full phenotype on the strain data sheet | ||
| 002591 | NOD.B10Sn-H2b/J | Repository- Live |
| This congenic strain serves as a diabetes-resistant control for comparison to the NOD/LtJ strain (Stock No. 001976). The diabetes resistant MHC H2b haplotype was transferred from C57BL/10J mice to the NOD/Lt strain. These mice exhibit some but not all of the immune dysfunctions of NOD/LtJ mice. They are useful in dissecting the role of MHC versus non-MHC genes in producing aberrant immunophenotypes. | ||
| 007934 | NOD.B6(PL)-Idd3C57BL/6/MrkTacJ | Repository- Live |
| This NOD congenic strain, commonly referred to as NOD.B6-Idd3, commonly referred to as NOD.B6-Idd3R450, is carrying Chromosome 3 alleles, rs3022959 through rs3140619, derived from strain C57BL/6 including the insulin dependent diabetes susceptibility 3 loci (Idd3). This NOD.B6 congenic strain is diabetes resistant, with approximately 10% of the females becoming diabetic by 250 days of age. Activated and non-activated thymocytes and splenocytes of this T1D protected stock produce more Il2 mRNA than T1D susceptible strains (Stock No's. 007930, 007931, and 007932). This congenic strain, one of a set of 5 strains (Stock No's. 007930, 007931, 007932
..... For more information please see the full phenotype on the strain data sheet | ||
| 006809 | NOD.B6-(D11Nds1-D11Mit41)/J | Repository- Live |
| Chromosome 11 congenic mice are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. The reported conclusion of diabetes resistance in this Chr 11 congenic is being re-evaluated now that the B6 contaminating genome on Chr 1 has been eliminated.
In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. It should be noted that the phenotype could vary from that originally described on a NOD/ShiLt genetic background. We will modify the strain description if necessary as published results become available.
This strain may be useful for identifying genes involved with diabetes resistance located within the Idd4 region of Chr 11. | ||
| 008223 | NOD.C3(B6)-Faslgld /LwnJ | Repository- Live |
| Mice homozygous for the Faslgld spontaneous mutation are viable and fertile. Homozygous males and females develop lymphadenopathy and systemic autoimmunity beginning at 8 weeks of age, but do not develop diabetes. The Lupus phenotype is accelerated in this strain when compared to the B6-Faslgldstrain. This mutant strain may be useful in the studies of apoptosis of lymphocytes, particularly T cells, and in studies of Lupus. In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized.. It should be noted that the phenotype could vary from that originally described. We will modify the strain description if necessary as published results become available. | ||
| 007932 | NOD.CAST-Idd3CAST/EiJ/MrkJ | Repository- Live |
| This NOD congenic strain, commonly referred to as NOD.CAST-Idd3, is carrying Chr 3 alleles, SNPs rs3022948 (7.43Mb) through rs13477164, (66.638Mb) derived from strain CAST/EiJ including the insulin dependent diabetes susceptibility 3 loci (Idd3). Diabetes onset and incidence among mice of this strain is reported to be similar to NOD/MrkTac. Thymocytes and splenocytes of this T1D susceptible stock produce 2 fold less Il2 mRNA than T1D protected strains (Stock No's. 007933 and 007934). This congenic strain, one of a set of 5 strains (Stock No's. 007930, 007931, 007933, 007934), has been useful to positionally clone Idd3 and to st
..... For more information please see the full phenotype on the strain data sheet | ||
| 007933 | NOD.CZI-Idd3CZECHI/EiJ/MrkTacJ | Repository- Live |
| This NOD congenic strain, commonly referred to as NOD.CZECH-Idd3, is carrying Chr 3 alleles, rs13477023 (20.01Mb) through rs13477134 (58.91Mb), derived from strain CZECH/EiJ including the insulin dependent diabetes susceptibility 3 loci (Idd3). Il2 exon 1 sequence and glycosylation pattern is similar to NOD/MrkTac. Surprisingly, the diabetes frequency of this strain of mice is identical to that of NOD.B6-Idd3 mice. Activated and non-activated thymocytes and splenocytes of this T1D protected stock produce 2 fold more Il2 mRNA than T1D susceptible strains (Stock No's. 007930, 007931, and 007932). However, the NOD.CZECH-Idd3 congenic produces more Il2 mRNA than the NOD.B6-Idd3 congenic. This congenic strain, one of a set of 5 strains (Stock No's For more information please see the full phenotype on the strain data sheet | ||
| 006023 | NOD.Cg-H2-Ab1tm1Gru Tg(CD4,HLA-DQA1,HLA-DQB1)N8Ell/EllJ | Repository- Live |
| This NOD congenic strain contains a targeted H2-Ab1 mutation also carries two transgenes: one expressing human CD4 under the regulation of the mouse Cd4 enhancer and a second expressing human HLA-DQ6. The latter transgene confers dominant protection to development of Type 1 diabetes in humans. These double transgenic, H2-Ab1-deficient mice are viable, fertile, normal in size, and free of both autoimmune diabetes and cardiomyopathy, a phenotype found in an NOD stock expressing an HLA-DQ8 transgene (Elliot JF et al. (2003).Proc Natl Acad Sci U S A 100(23):13447-52). By 55 weeks of age, 100% of the H2-Ab1-deficient, DQ6 transgenic mice develop thyroiditis and thyroid autoantibodies. Of these, 25% develop thyroid gland enlargement and goiter, and a subset of these animals develops thyroid failure with elevated serum TSH levels. This model is useful for studying autoimmune thyroid disease and to understand the role of MHC class II in autoimmunity. | ||
| 006608 | NOD.Cg-Igh-6tm1Cgn Tg(IghelMD4)4Ccg/DvsJ | Repository- Live |
| NOD.Cg-Igh-6tm1Cgn Tg(IghelMD4)4Ccg/DvsJ (NOD.IgHEL Igh-6-deficient) mice are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. Because these mice are Igh-6-deficient, they do not express endogenous IgM. All B lymphocytes in NOD.IgHEL Igh-6-deficient mice express Ig molecules specific for hen egg lyzozyme (HEL). There is no significant difference in the total number of B and T lymphocytes between NOD.IgHEL Igh-6-deficient and NOD.IgHEL (Stock No. 006345) mice. The incidence of diabetes in transgenic vs. non-transgenic NOD.Igh-6-deficient mice is similar by 21 weeks of age, (16.7% vs. 13.6%, respectively). Histological evaluation of 12 week old NOD.IgHEL Igh-6-deficient mice shows that most mice have low levels of insulitis compared to NOD/ShiLt control mice, although an occasional animal had extensive insulitis. In
..... For more information please see the full phenotype on the strain data sheet | ||
| 007840 | NOD.Cg-Prkdcscid Tg(Ins2-CD86)12B70Flv/FswJ | Repository- Live |
| Tg(Ins2-CD86)12B7 mice homozygous for the Prkdcscid mutation are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. Transgenic mice express the human CD86 T cell co-stimulatory protein under the control of the rat insulin promoter (Ins2). RT-PCR analysis detects human CD86 mRNA expression in the pancreas. Very low expression levels are also detected in the kidney and thymus of some but not all transgenic mice. Immunohistochemistry indicates that transgenic CD86 protein expression is restricted to the Islets of Langerhans. Transgenic, Prkdcscid homozygous mice lack functional T cells and B cells, and do not become diabetic.
In the absence of the Prkdcscid mutation, NOD-Tg(Ins2-CD86), transgenic mice experience accelerated diabetes. Diabetes onset in male and female transgenic NOD-Tg(Ins2-CD86) mice starts at 8 weeks of age and 85-90% of the mice ultimately become d
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| 006605 | NOD.Cg-Prkdcscid Emv30b Tg(HLA-A/H2-D/B2M)1Dvs/DvsJ | Repository- Live |
| Although NOD mice that carry this transgene (Stock No. 006604) develop diabetes significantly earlier than do NOD/ShiLtDvs (NOD) controls, this transgenic strain harbors the Prkdcscid mutation (characterized by an absence of functional T cells and B cells), and therefore does not become diabetic. This strain is useful for adoptive transfer experiments, and as a source of insulitis free pancreatic islets. | ||
| 004460 | NOD.Cg-Tg(TcraBDC2.5)1Doi Tg(TcrbBDC2.5)2Doi/DoiJ | Repository- Live |
| NOD.Cg-Tg(TcraBDC2.5)1Doi Tg(TcrbBDC2.5)2Doi/DoiJ mice carry both rearranged TCR alpha and beta genes from the cytotoxic CD4+ T cell clone BDC-2.5. When paired with a homozygous Rag1tm1Mom mutation (such as in Stock No. 003729), recombination of endogenous TCR and Ig is prevented so that mature T cells in these mice express only the BDC2.5 TCR. On the NOD background, mice carrying the transgenes have a reduced incidence of diabetes relative to NOD/ShiLtJ controls (12% incidence at age 30 weeks). When coupled with the homozygous Rag1tm1Mom mutation, mice develop diabetes extremely early (mean age of 25 days). (Katz et al 1993, Gonzalez et al 2001, Mombaerts et al 1992) | ||
| 007769 | NOD.FVB-Tg(Igh-6-Cd80)1Gjf/JbsJ | Repository- Live |
| Transgenic mice are viable, fertile, normal in size, normoglycemic and do not display any gross physical or behavioral abnormalities. High levels of the transgene are expressed on B cells, but not on T cells. At 30 weeks of age transgenic mice are diabetes resistant and insulitis was significantly reduced when compared with wildtype NOD controls. When compared to wildtype NOD controls, the circulating B cells in congenic NOD transgenic mice is 2-3 fold lower in 2 week old mice and 10 fold lower in 5-6 week old mice and persists throughout life. Significantly reduced percentage of B cells were found in the spleen and bone marrow. Analysis of bone marrow shows the more mature B cell subsets (B220+, IgM+) are affected. Elisa tests indicate reduced circulating levels of all Ig types, Igh-6 (IgM), Igh-3 (IgG2b), and Ighg1 (IgG1) in the serum of transgenic mice. MHC class II expression of splenic B cells was significantly increased by more than 2 fold, indicating feature
..... For more information please see the full phenotype on the strain data sheet | ||
| 008056 | NOD.L-(Csf2-D11Mit339)/McdfJ | Repository- Live |
| This NOD congenic strain, commonly referred to as NOD.Lc11e or DR3e carries Chromosome 11 alleles, D11Mit164 (56Mb) through D11Mit339 (63Mb) derived from C57L/J including a small part of Idd4 that includes candidate gene Csf2. Diabetes incidence in this strain is reported to be about 53% in females compared to 70% in female NOD control mice. (Davoodi-Semiromi et al 2007). There appear to be multiple diabetes resistant regions (Idd4) on Chromosome 11, therefore, this strain is useful to identify candidate genes associated with diabetes resistance and to positionally clone the Idd4 resistant loci. | ||
| 008060 | NOD.L-(D11Mit314-D11Mit339)(D11Mit132-D11Mit42)/McdfJ | Repository- Live |
| This NOD congenic strain, commonly referred to as NOD.Lc11j or DR3j carries Chromosome 11 alleles, D11Mit314 (51Mb) through D11Mit339 (63Mb) and D11Mit132 (86Mb) through D11Mit42 (113Mb) derived from C57L/J, which includes candidate gene Csf2 and Stat5a, Stat5b and Stat3. Diabetes incidence in this strain is reported to be about 12% in females compared to 70% in female NOD control mice. (Davoodi-Semiromi et al. 2007). This strain is useful to further study the role of Csf2, Stat5a, Stat5b and Stat3 in autoimmune diabetes; to identify additional candidate diabetes resistant genes and to positionally clone the Idd4 diabetes resistant loci. | ||
| 008061 | NOD.L-(D7Mit253-D7Mit242)/McdfJ | Repository- Live |
| This NOD congenic strain, commonly referred to as NOD.Lc7 or DR4, carries Chr. 7 alleles, D7Mit253 (115Mb) through D7Mit242 (138Mb), derived from C57L/J and is distal to either Idd7 or Idd27. Diabetes incidence in this diabetes resistant strain is reported to be 10% in females and 0% in males compared to 70% in female and 40% in male NOD/Bdc controls. Both males and females develop widespread islet associated infiltrates and invasive insulitis, although the beta cell mass and insulin content are well maintained. NOD.Lc7 neonates injected with T-cells from old NOD mice were resistant to diabetes, however 100% of the female and 38% of the male NOD recipients receiving T cells from non diabetic, 5+ month old NOD.Lc7 mice developed diabetes starting at 12 weeks of age. This strain is useful for identifying candidate genes within this new and unique Idd region and to eventually positionally clone the newly identified resistance loci. | ||
| 008053 | NOD.L-(D11Mit314-D11Mit42)/McdfJ | Repository- Live |
| This NOD congenic strain, commonly referred to as NOD.Lc11 or DR3, carries Chromosome 11 alleles, D11Mit314 (51Mb) through D11Mit42 (112Mb), derived from C57L/J including Idd4 and a candidate gene Csf2. Diabetes incidence in this diabetes resistant strain is reported to be 9% in the females and 0% in males compared to 70% in female and 40% in male NOD/Bdc control mice. NOD.Lc11 mice develop mild periductular infiltrates early in life and by 44 weeks of age histological analysis indicates healthy islet beta cells and normal amounts of stored insulin. Neonates injected with T cells from 8-week-old prediabetic NOD females and from old NOD mice were resistant to diabetes by 25 weeks of age. Splenic and lymph node derived T cells from NOD.Lc11 mice fail to cause diabetes or beta cell damage in NOD.scid neonatal mice, however 6 weeks post transfer the recipients develop severe invasive insulitis. Adult NOD.scid females that received T cells from NOD.Lc11 mice
..... For more information please see the full phenotype on the strain data sheet | ||
| 004483 | NOD.NON-Thy1a/1LtJ | Repository- Live |
| 002032 | NOD.SW-H2q/J | Repository- Live |
| This congenic strain carries the diabetes-resistant MHC from the from SWR/J (Stock No. 000689) and is used as a comparison to the NOD/ShiLtJ (Stock No. 001976). These mice exhibit some but not all of the immune dysfunctions of NOD/ShiLtJ mice. These mice are useful for dissecting the role of MHC versus non-MHC genes in producing aberrant immunophenotypes. | ||
| 007930 | NOD.SWR-Idd3SWR/J/MrkJ | Repository- Live |
| This NOD congenic strain, commonly referred to as NOD.SWR-Idd3, is carrying Chr 3 alleles, SNPs rs13476974 (11.10Mb) through rs13477217 (78.79Mb), derived from strain SWR/J including the insulin dependent diabetes susceptibility 3 loci (Idd3). Diabetes onset and incidence among mice of this strain reported reported to be similar to NOD/MrkTac. Thymocytes and splenocytes of this T1D susceptible stock produce 2 fold less Il2 mRNA than T1D protected strains (Stock No's. 007933 and 007934). This stock has been useful to positionally clone Idd3 and to study the biological effects of variation of genes within the Idd3 region, specifically the Il2 gene and continue to be valued for studying long-range chromosome remodeling. | ||
| 005328 | NOD/ShiLt-Tg(Cd4-DsRed)4Lt/J | Repository- Live |
| The donating investigator reports that hemizygous transgenic mice are viable, fertile and normal in size. FACS analysis of splenic lymphocytes shows transgenic expression in 36% of CD4+ and 6% of CD8+ T-cells and minimal expression (background levels) in B cells and macrophages. When compared to wild-type NOD/ShiLt mice, the diabetes incidence is lower (50%) and diabetes onset is delayed. Adoptive transfer experiments with splenocytes and bone marrow from hemizygous CD4-DsRed transgenic mice does not confer diabetes protection on NOD inbred mice, suggesting that the agent of protection is not dependent on hematopoietic cells. No homozygous transgenic mice have been identified in litters produced from hemizygote intercrosses, suggesting that homozygotes are not viable. This strain is useful for tracking resting and activated T cells in vivo and in vitro. | ||
| 005334 | NOD/ShiLt-Tg(Cd4-EGFP)1Lt/J | Repository- Live |
| Homozygous transgenic mice are viable, fertile, normal in size and do not exhibit any gross physical or behavioral abnormalities. The donating investigator reports uniform transgenic expression, about 81% of inactivated or resting CD8+ T cells and CD4+ T cells, with minimal expression in B cells (2.3%) and macrophages (1.5%). Over a three day period following activation in vitro with anti-CD3, gating on live populations of CD4+ and CD8+ subsets show continued GFP expression in both. However, there is a greater diminution of GFP fluorescence in the activated CD8+ T population by day three in vitro. Diabetes onset is similar to wild-type NOD/ShiLt mice. These CD4-GFP transgenic mice may be useful for fluorescent monitoring of T cells both in vivo and in vitro. | ||
| 006604 | NOD/ShiLtDvs-Tg(HLA-A/H2-D/B2M)1Dvs/J | Repository- Live |
| This transgenic NOD mouse model, commonly referred to as NOD.HHD, develops significantly accelerated diabetes onset compared to NOD/ShiLtDvs (NOD) inbred mice.
When transgenic mice are bred to NOD-B2m-deficient mice (e.g. Stock No. 002309), which completely lack CD8+ T cells, CD8+ T cells are restored in the double mutant mice, but at significantly lower levels than in NOD inbred mice. FACS analysis indicates that the transgenic NOD-B2m-deficient mice express only the HLA-A2.1/H2-Db chimeric class I molecule. In contrast to NOD.B2mtm1Unc females, which are diabetes free, 55% of the transgenic NOD B2m-deficient females develop diabetes by 30 weeks of age. Insulitis scores determined by histological examination are similar between the NOD double mutant mice and NOD/ShiLtDvs inbred mice, and cultured pancreatic islets from transgenic NOD B2m-deficient mice an
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| 002423 | NON/ShiLtJ | Repository- Live |
| Although closely related to NOD mice, NON mice contain a diabetes resistant MHC haplotype (H2nb1 = Kb, Anb1, Ek, Db). The name was derived from "Non-Obese Non-diabetic"; however, NON/ShiLtJ mice should not be considered "normal." They carry the retinal degeneration (Pde6b) mutation and exhibit certain tendencies toward autoimmune disease. This strain maintains a low plasma insulin level, which may account in part why certain loci from NON/ShiLt can enhance development of autoimmune type 1 diabetes in segregating hybrid mice following outcross to NOD/ShiLtJ. The NON strain-characteristic immunologic abnormalities include perivascular/periductular leukocyte infiltration into the pancreas and submandibular salivary glands, and T lymphocytopenia evident by 20 weeks of age in spleen. NON/ShiLt mice clearly harbor genes predisposing to type 2 diabetes, as evidenced by early impaired glucose tolerance in males and females, d
..... For more information please see the full phenotype on the strain data sheet | ||
| 006866 | STOCK Tg(Ins1-DsRed*T4)32Hara/J | Repository- Live |
| Mice hemizygous for this "MIP-RFP" transgene are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. These transgenic mice express the DsRed.T4 variant of Enhanced Red Fluorescent Protein under the control of mouse insulin I promoter (MIP). Fluorescence is detected in tissues where insulin I is normally expressed; fluorescent protein expression in pancreatic beta-cells is evident from embryonic day (E)13.5 through adulthood. Transgenic mice exhibit normal glucose tolerance and pancreatic insulin levels. The human growth hormone sequence in the transgene is designed to enhance expression of the fluorescent protein. Although the expression of this sequence in this strain has not been characterized, the sequence is not expressed in a similarly constructed transgenic strain (see Stock No. 006864). This mutant mouse strain may be useful in studies of pancreatic development and pancreatic b
..... For more information please see the full phenotype on the strain data sheet | ||
| 006784 | STOCK Tg(Ins1-ECFP)24Hara/J | Repository- Live |
| Mice hemizygous for this "MIP-CFP" transgene are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. These transgenic mice express the Cerulean variant of Enhanced Cyan Fluorescent Protein under the control of mouse insulin 1 promoter (MIP). Fluorescence is detected in tissues where insulin I is normally expressed; fluorescent protein expression in pancreatic beta-cells is evident from embryonic day (E)13.5 through adult. The fluorescence expression pattern observed in this strain is similar to the patterns seen in other stocks that express fluorescent proteins from the MIP promoter (see Stock No. 006864 and Stock No. 006866). The human growth hormone sequence in the transgene is designed to enhance expression of the fluorescent protein. Although the expression of this sequence in this strain has not been characterized, the seque
..... For more information please see the full phenotype on the strain data sheet | ||
| 005715 | B6.Cg H2g7-Tg(Ins2-CD80)3B7Flv/LwnJ | Repository-Cryopreserved |
| Transgenic mice are characterized by pancreatic beta cells that express a rat insulin promoter (Ins2) regulated transgene encoding the human CD80 T cell co-stimulatory molecule. These mice are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. Better than 70% of the B6.H2g7 transgenic mice become diabetic by 30 weeks of age compared the control B6.H2g7 which does not develop insulitis or diabetes. Spleens of diabetic B6.H2g7 transgenic mice used in adoptive transfer experiments transfer diabetes to NOD.scid/RIP-B7.1 and irradiated non-diabetic B6.Cg H2g7-Tg(Ins2-CD80)3B7Flv/LwnJ mice, yet failed to transfer disease to NOD.scid, B6.scid, CB17.scid, or irradiated B6/RIP-B7.1. B6.Cg H2g7-Tg(Ins2-CD80)3B7Flv/LwnJ provides a tool for studying mechanisms of loss of tolerance in potentially diabetogenic CD8 T-cells. | ||
| 003068 | B6.NOD-(Csf2-D11Mit42) (D17Mit21-D17Mit10)/J | Repository-Cryopreserved |
| This strain is doubly congenic for a 19 cM segment of Chr 17 (called c17 in the reference below) extending from D17Mit21through D17Mit10and including the major histocompatibility complex, H2,and the insulin dependent diabetes susceptibility locus Idd1and for a 42 cM segment of Chr 11 (called c11 by Yui et al.)extending from Csf2(colony stimulating factor 2 (granulocyte-macrophage)) through D11Mit42and including the insulin dependent diabetes susceptibility locus Idd4.No information has been published for this double congenic strain. However, upon histologic examination of the pancreas, a significantly higher percentage of B6.NOD-(D17Mit21-D17Mit10) singly congenic mice than of C57BL/6J control mice were found to exhibit periinsulitis, and more extensive mononuclear cell infiltrates were observed in the pancreata of these mice. The pancreatic infiltrates were not associated specifically with the islets. Insulitis (intraislet
..... For more information please see the full phenotype on the strain data sheet | ||
| 003065 | B6.NOD-(Csf2-D11Mit42)/J | Repository-Cryopreserved |
| This strain is congenic for a 42 cM segment of Chr 11 extending from Csf2(colony stimulating factor 2, granulocyte-macrophage) through D11Mit42that includes the insulin dependent diabetes susceptibility locus Idd4.The name given this segment in the primary reference is c11. Upon histological examination of the pancreas, the incidence and severity of periinsulitis (perivascular, periductal and/or periislet infiltration by mononuclear cells) in B6.NOD-(Csf2-D11Mit42) mice were found to be similar to those in C57BL/6 controls. | ||
| 003069 | B6.NOD-(D1Mit3-Bcl2) (D17Mit21-D17Mit10)/LtJ | Repository-Cryopreserved |
| This strain is doubly congenic for a 19 cM segment of Chr 17 (called c17 in the reference below) extending from D17Mit21through D17Mit10and including the major histocompatibility complex, H2,and the insulin dependent diabetes susceptibility locus Idd1and for a 44 cM segment of Chr 1 (called c1c by Yui et al.)extending from D1Mit3through Bcl2(B-cell leukemia/lymphoma 2) and including Idd5(insulin dependent diabetes susceptibility 5). No information has been published for this double congenic. However, upon histologic examination of the pancreas, a significantly higher percentage of both B6.NOD-D1Mit3-Bcl2 (Idd5)and B6.NOD-D17Mit21-D17Mit10 (H2g7, Idd1)singly congenic mice than of C57BL/6J control mice were found to exhibit periinsulitis, and more extensive mononuclear cell infiltrates were observed in the pancreas of these mice. The pancreatic infiltrates were not associated specifically with the islets. In
..... For more information please see the full phenotype on the strain data sheet | ||
| 003062 | B6.NOD-(D1Mit3-Bcl2)/J | Repository-Cryopreserved |
| This strain is congenic for a 44 cM segment of Chr 1 extending from D1Mit3through Bcl2(B-cell leukemia/lymphoma 2) that includes Idd5(insulin dependent diabetes susceptibility 5). The name given this segment in the primary reference is c1c. Upon histologic examination of the pancreas, a significantly higher percentage of B6.NOD-(D1Mit3-Bcl2) congenic mice than of C57BL/6J control mice were found to exhibit periinsulitis, and more extensive mononuclear cell infiltrates were observed in the pancreata of these mice. The pancreatic infiltrates were not associated specifically with the islets. Insulitis (intraislet infiltration) was extremely rare, and no more than one affected islet was observed in a single animal, even in cases where extensive perivascular/periductal infiltrates existed. Female B6.NOD-(D1Mit3-Bcl2) mice exhibited pancreatic infiltration at twice the frequency of males; female NOD mice are more susceptible than males to both insulitis and
..... For more information please see the full phenotype on the strain data sheet | ||
| 003867 | B6.NOD-(D1Mit5.1-D1Mit159)/LtJ | Repository-Cryopreserved |
| 003071 | B6.NOD-(D1Mit5.1-D1Mit15) (D17Mit21-D17Mit10)/J | Repository-Cryopreserved |
| This strain is doubly congenic for a 19 cM segment of Chr 17 (called c17 by Yui et al.) extending from D17Mit21through D17Mit10and including the major histocompatibility complex, H2,and the insulin dependent diabetes susceptibility locus Idd1and for a 47 cM segment of Chr 1 (called c1t by Yui et al.) extending from D1Mit5through D1Mit15and including Idd5(insulin dependent diabetes susceptibility 5). No information has been published for this double congenic strain. However, upon histologic examination of the pancreas, a significantly higher percentage of both B6.NOD-(D1Mit5-D1Mit15) and of B6.NOD-(D17Mit21-D17Mit10) singly congenic mice than of C57BL/6J control mice were found to exhibit periinsulitis, and more extensive mononuclear cell infiltrates were observed in the pancreata of these mice. The pancreatic infiltrates were not associated specifically with the islets. Insulitis (intraislet infiltration) was
..... For more information please see the full phenotype on the strain data sheet | ||
| 003866 | B6.NOD-(D1Mit5.1-D1Mit15)/J | Repository-Cryopreserved |
| This strain is congenic for a 47 cM segment of Chr 1 extending from D1Mit5 through D1Mit15 that includes Idd5 (insulin dependent diabetes susceptibility 5). The name given this segment in the primary reference is c1t. Upon histologic examination of the pancreas, a significantly higher percentage of B6.NOD-D1Mit5-D1Mit15 congenic mice than of C57BL/6J control mice were found to exhibit periinsulitis, and more extensive mononuclear cell infiltrates were observed in the pancreata of these mice. The pancreatic infiltrates were not associated specifically with the islets. Insulitis (intraislet infiltration) was extremely rare, and no more than one affected islet was observed in a single animal, even in cases where extensive perivascular/periductal infiltrates existed. Female B6.NOD-D1Mit5-D1Mit15 mice exhibited pancreatic infiltration at twice the frequency of males; female NOD mice are more susceptible than males to both insulitis and diabetes. | ||
| 003064 | B6.NOD-(D2Mit274-D2Mit343)/J | Repository-Cryopreserved |
| This strain is congenic for an 32 cM segment of Chr 2 extending from D2Mit274through D2Mit343that includes the insulin dependent diabetes susceptibility locus Idd13(Myrick C, Leiter EH, Langley SH. 2000. Personal communication.) | ||
| 003067 | B6.NOD-(D3Mit132-Tshb) (D17Mit21-D17Mit10)/J | Repository-Cryopreserved |
| This strain is doubly congenic for a 19 cM segment of Chr 17 (called c17 by Yui et al.) extending from D17Mit21through D17Mit10and including the major histocompatibility complex, H2,and the insulin dependent diabetes susceptibility locus Idd1and for a 43 cM segment (called c3 by Yui et al.) of Chr 3 extending from D3Mit132through Tshb(thyroid stimulating hormone, beta subunit) and including the insulin dependent diabetes susceptibility loci Idd3and Idd10.No information has been published for this doubly congenic strain. However, upon histologic examination of the pancreas, a significantly higher percentage of B6.NOD-(D17Mit21-D17Mit10) singly congenic mice than of C57BL/6J control mice were found to exhibit periinsulitis, and more extensive mononuclear cell infiltrates were observed in the pancreata of these mice. B6.NOD-(D3Mit132-Tshb) singly congenic females also demonstrated a higher incidence of per
..... For more information please see the full phenotype on the strain data sheet | ||
| 003059 | B6.NOD-(D3Mit132-Tshb)/J | Repository-Cryopreserved |
| This strain is congenic for a 43 cM segment of chromosome 3 extending from D3Mit132through Tshb(thyroid stimulating hormone, beta subunit) that includes the diabetes susceptibility loci Idd3and Idd10 (which has been subsequently refined into three diabetes susceptibility loci: Idd10, Idd17, and Idd18). The name given this segment in the primary reference is c3. Upon histologic examination of the pancreas, B6.NOD-(D3Mit132-Tshb) female mice exhibited somewhat higher incidence of periinsulitis (perivascular, periductal and/or periislet infiltration by mononuclear cells) than did C57BL/6J controls, but the difference was not statistically significant. Female B6.NOD-(D3Mit132-Tshb) mice had twice the incidence of periinsulitis as males; female NOD mice are more susceptible than males to both insulitis and diabetes. | ||
| 003066 | B6.NOD-(D6Mit54-D6Mit14) (D17Mit21-D17Mit10)/J | Repository-Cryopreserved |
| This strain is doubly congenic for a 19 cM segment of Chr 17 (called c17 in Yui et al.) extending from D17Mit21through D17Mit10and including the major histocompatibility complex, H2,and the insulin dependent diabetes susceptibility locus Idd1and for a 24 cM segment (called c6 by Yui et al.)of Chr 6 extending from D6Mit54through D6Mit14and including the insulin dependent diabetes susceptibility locus Idd6.No information has been published for this double congenic strain. However, upon histologic examination of the pancreas, a significantly higher percentage of B6.NOD-(D17Mit21-D17Mit10) singly congenic mice than of C57BL/6J control mice were found to exhibit periinsulitis, and more extensive mononuclear cell infiltrates were observed in the pancreata of these mice. The pancreatic infiltrates were not associated specifically with the islets. Insulitis (intraislet infiltration) was extremely rare, and no more than one a
..... For more information please see the full phenotype on the strain data sheet | ||
| 003063 | B6.NOD-(D6Mit54-D6Mit14)/J | Repository-Cryopreserved |
| This strain is congenic for a 24 cM segment of Chr 6 extending from D6Mit54through D6Mit14that includes the insulin dependent diabetes susceptibility locus Idd6.The name given this segment in the primary reference is c6. Upon histologic examination of the pancreas, the incidence and severity of periinsulitis (perivascular, periductal and/or periislet infiltration by mononuclear cells) of B6.NOD-(D6Mit54-D6Mit14) mice were found to be similar to those of C57BL/6 controls. | ||
| 005713 | C.Cg-Tg(Ins2-CD80)3B7Flv/LwnJ | Repository-Cryopreserved |
| Transgenic mice are characterized by pancreatic beta cells that express a rat insulin promoter (Ins2) regulated transgene encoding the human CD80 T cell co-stimulatory molecule. These mice are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. Approximately 10% of the BALB transgenic mice become diabetic by 30 weeks of age compared the control BALBs which are diabetes resistant. Spleens of diabetic BALB transgenic mice used in adoptive transfer experiments do not transfer diabetes to NOD.scid/RIP-B7.1. C.Cg-Tg(Ins2-CD80)3B7Flv/FswJ provides a tool for studying mechanisms for loss of tolerance in potentially diabetogenic CD8 T-cells. | ||
| 002980 | C57BL/6-Tg(Cd152Ig)1Jbs/J | Repository-Cryopreserved |
| A soluble form of the CD152 antigen (CTLA4Ig)is expressed under the control of the K14 promoter that is primarily active in the skin, but also thymus and tongue. The animal produces blood circulating levels of CTLA4Ig that are easily detectable by ELISA or functional assays. | ||
| 002349 | CBcNO6/LtJ | Repository-Cryopreserved |
| Neither spontaneous IDDM nor significant insulitis has been observed in any of the NOcCB or CBcNO recombinant congenic strains. Histologic analysis revealed leukocyte infiltration of the submandibular salivary glands (sialitis) of aging mice. Mice of these strains also developed pancreatic infiltrates, but these were limited to the perivascular and periductal regions of the pancreas (peri-insulitis) and did not focus on the islets. All strains exhibited strong resistance to induction of both IDDM and insulitis by a cyclophosphamide treatment regimen that causes diabetes within two weeks of the second dose in 90% of female NOD mice. | ||
| 003052 | CBcNO7A/LtJ | Repository-Cryopreserved |
| Neither spontaneous IDDM nor significant insulitis has been observed in any of the NOcCB or CBcNO recombinant congenic strains. Histologic analysis revealed leukocyte infiltration of the submandibular salivary glands (sialitis) of aging mice. Mice of these strains also developed pancreatic infiltrates, but these were limited to the perivascular and periductal regions of the pancreas (peri-insulitis) and did not focus on the islets. All strains exhibited strong resistance to induction of both IDDM and insulitis by a cyclophosphamide treatment regimen that causes diabetes within two weeks of the second dose in 90% of female NOD mice. | ||
| 003053 | CBcNO7B/LtJ | Repository-Cryopreserved |
| Neither spontaneous IDDM nor significant insulitis has been observed in any of the NOcCB or CBcNO recombinant congenic strains. Histologic analysis revealed leukocyte infiltration of the submandibular salivary glands (sialitis) of aging mice. Mice of these strains also developed pancreatic infiltrates, but these were limited to the perivascular and periductal regions of the pancreas (peri-insulitis) and did not focus on the islets. All strains exhibited strong resistance to induction of both IDDM and insulitis by a cyclophosphamide treatment regimen that causes diabetes within two weeks of the second dose in 90% of female NOD mice. | ||
| 003054 | CBcNO7C/LtJ | Repository-Cryopreserved |
| Neither spontaneous IDDM nor significant insulitis has been observed in any of the NOcCB or CBcNO recombinant congenic strains. Histologic analysis revealed leukocyte infiltration of the submandibular salivary glands (sialitis) of aging mice. Mice of these strains also developed pancreatic infiltrates, but these were limited to the perivascular and periductal regions of the pancreas (peri-insulitis) and did not focus on the islets. All strains exhibited strong resistance to induction of both IDDM and insulitis by a cyclophosphamide treatment regimen that causes diabetes within two weeks of the second dose in 90% of female NOD mice. | ||
| 003055 | CBcNO7D/LtJ | Repository-Cryopreserved |
| Neither spontaneous IDDM nor significant insulitis has been observed in any of the NOcCB or CBcNO recombinant congenic strains. Histologic analysis revealed leukocyte infiltration of the submandibular salivary glands (sialitis) of aging mice. Mice of these strains also developed pancreatic infiltrates, but these were limited to the perivascular and periductal regions of the pancreas (peri-insulitis) and did not focus on the islets. All strains exhibited strong resistance to induction of both IDDM and insulitis by a cyclophosphamide treatment regimen that causes diabetes within two weeks of the second dose in 90% of female NOD mice. | ||
| 005739 | NOD-Tg(H2-Ea-Ins2)1Wehi/WehiJ | Repository-Cryopreserved |
| Transgenic mice are viable, fertile, normal in size, normoglycemic and do not display any gross physical or behavioral abnormalities. RT/PCR indicates transgene expression in the spleen and thymus. Blood glucose levels of transgenic and non-transgenic littermates are identical. 90-98 % of the transgenic islets of females and males are insulitis free. Transgenic mice do not develop spontaneous diabetes and are resistant to cyclophosphamide-induced diabetes. Sialitis is not statistically different between transgenic and littermate controls (French MB, Diabetes 1997 46:34-9). Transgenic bone marrow transplanted into 4-week-old irradiated NOD female’s almost entirely prevented diabetes compared to control NOD to irradiated NOD transplants, which have an overall diabetes incidence similar to untreated controls. Thymoma incidence was similar in both irradiated groups.(Steptoe RJ, J Clin Invest 2003 111:1357-63) This model may be helpful for looking at antigen speci ..... For more information please see the full phenotype on the strain data sheet | ||
| 005020 | NOD-Tg(Igh-6/Igh-V281)3Jwt/JwtJ | Repository-Cryopreserved |
| The double transgenic produced by crossing this stock with Stock No. 005018 serves as a control to the double transgenic which results from crossing Stock No. 005018 with Stock No. 005019. | ||
| 005522 | NOD-Tg(Ins2*Y16A)1Ell/GseJ | Repository-Cryopreserved |
| Expression has been reported in the pancreatic islets and thymus of NOD mice carrying the Tg(Ins2*Y16A)1Ell mutation. Approximately 75% of line B female transgenic mice become diabetic in the presence of native insulin genes by 35 weeks of age. NOD female transgenic mice lacking both Ins1 and Ins2 fail to produce insulin autoantibodies, and there is no diabetes or insulitis at 26 weeks of age, but sialitis is present. Donating investigator reports male transgenics lacking both Ins1 and Ins2 develop metabolic diabetes before 10 weeks of age. In contrast, transgenic female mice in the presence of Ins1 and lacking Ins2 develop diabetes in 75% of the animals by 25 weeks of age (Nakayama et al, 2004, 2005). Donating investigator reports line B transgenics have lower expression levels than line F and that male transgenics lacking both Ins1 and Ins2 develop metabolic diabetes before 10 weeks of age. NOD-Tg(Ins2*Y16A)1Ell/GseJ is usefu
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| 005523 | NOD-Tg(Ins2*Y16A)3Ell/GseJ | Repository-Cryopreserved |
| Expression has been reported in the pancreatic islets and thymus of NOD mice carrying the Tg(Ins2*Y16A)3Ell mutation. Approximately 15% of line F female transgenic mice become diabetic in the presence of native insulin genes by 35 weeks of age. NOD female transgenic mice lacking both Ins1 and Ins2 fail to produce insulin autoantibodies, and there is no diabetes or insulitis at 26 weeks of age, but sialitis is present. In contrast, transgenic mice in the presence of Ins1 and lacking Ins2 develop diabetes in 75% of the animals by 25 weeks of age (Nakayama et al, 2004, 2005). NOD-Tg(Ins2*Y16A)3Ell/GseJ is useful to study insulin-reactive autoimmunity. | ||
| 005356 | NOD.129(B6)-B2mtm1Unc Ciitatm1Ccum/BhsJ | Repository-Cryopreserved |
| NOD.129(B6)-B2mtm1UncC2tatm1Ccum/BhsJ is homozygous for linkage markers delineating Idd1-5, 7-10 and 13-15 loci of NOD origin and do not become diabetic. Histology indicates normal islet tissue structure with no cellular infiltration. Islets are intact and produce insulin. FACs analysis of peripheral blood cells of mice homozygote for B2mtm1Unc and C2tatm1Ccum confirmed the absence of MHC I or MHC II cell surface expression, reduced peripheral T-cell populations, deficiency of CD4+ and CD8+ T-cells and there is no difference in B-cell numbers when compared with wild-type controls. Additionally, B2mtm1Unc,C2tatm1Ccum double homozygous animals exhibit lower IgG titers and higher IgM titers than wild-type controls. Diabetic NOD females receiving purified islets from NOD.129(B6)-B2mtm1UncC2tatm1Ccum/BhsJ transplanted under the kidney capsule remain normal
..... For more information please see the full phenotype on the strain data sheet | ||
| 005144 | NOD.129(B6)-Ctla4tm1All/DoiJ | Repository-Cryopreserved |
| Heterozygous Ctla4tm1All mice are viable, fertile, and normal in size and exhibit diabetes incidence comparable to NOD. Ctla4tm1All homozygous mice on various backgrounds, including C57BL/6, BALB/c, 129 and NOD, die at 3-4 weeks of age due to massive polyclonal expansion of T-cells and massive lymphocyte infiltration into non-lymphoid organs, such as heart, liver, lung and pancreas. Treatment with murine Ctla4Ig or depletion of CD4+ T-cells blocks this lymphoproliferative disease. Splenic and lymph node T-cells display an activated phenotype characterized as CD69+, CD25+, CD44hi, Mel14lo, CD45RBlo and Sca1hi and have down regulated the TCR. Lymph node and spleen cells cultured from Ctla4tm1All homozygous mice spontaneously proliferate while wild-type controls do not. Cells from whole lymph nodes or purified T-cells are unresponsive to anti CD28mAb stimu
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| 004673 | NOD.129(B6)-Rag1tm1Mom Cd80tm1Shr/JbsJ | Repository-Cryopreserved |
| The NOD.129(B6)Rag1tm1MomCd80tm1Shr/JbsJ homozygous mice fail to produce T or B cells. Mice homozygous for both Rag1tm1Mom and Cd80tm1Shr are viable and fertile and exhibit no signs of diabetes due to the absence of lymphocytes. On the NOD background Cd80tm1Shr alone exacerbates diabetes onset when compared to standard NOD controls. When injected with proteolipid protein in Complete Freund's Adjuvant, NOD mice homozygous for the Cd80tm1Shr/JbsJ mutation alone develop similar though slightly milder, experimental autoimmune encephalomyelitis (EAE) when compared with NOD controls. NOD.129(B6)-Rag1tm1MomCd80tm1Shr/JbsJ are valuable for unraveling the co-stimulatory pathways of T cell activation as it relates to autoimmune diseases and organ transplantation. | ||
| 005352 | NOD.129-(D19Mit10-D19Mit54)/GseJ | Repository-Cryopreserved |
| This NOD/ShiLt congenic strain, commonly called NOD.Ins1 control, is carrying Chromosome 19 alleles derived from strain 129S1/SvImJ at the Ins1 loci. Diabetes onset and incidence among NOD.129-(D19Mit10-D19Mit54)/GseJ congenic mice is similar to NOD, Nakayama M, Nature 2005 435:220-3. This strain is useful as a control for the exploration of Ins1 in the context of the NOD congenic Ins1 targeted mutation (Stock No. 005035). | ||
| 005353 | NOD.129-(D7Mit105-D7Mit223)/GseJ | Repository-Cryopreserved |
| This NOD/ShiLt congenic strain, commonly called NOD.Ins2 control, is carrying Chromosome 7 alleles derived from strain 129S1/SvImJ at the Ins2 loci. Diabetes onset and incidence among NOD.129-(D7Mit105 -D7Mit223)/GseJ congenic mice is similar to NOD. (Nakayama M, Nature 2005 435:220-3) This strain is useful as a control for the exploration of Ins2 in the context of the NOD congenic Ins2 targeted mutation (Stock No. 005036). | ||
| 002309 | NOD.129P2(B6)-B2mtm1Unc/J | Repository-Cryopreserved |
| Mice homozygous for the B2mtm1Unc targeted mutation have little if any MHC class I protein expression on the cell surface. There are few CD8+ cytotoxic T-cells and under some circumstances a compensatory increase in CD4+ cytotoxic T-cells. Immune responses involving CD8+ T-cells are severely deficient providing a model to assess the role of CD8+ cells and class I MHC in various experimental systems. Other traits of B2M deficient mice include: NK cell deficiency, NK1+ T cells deficiency and decreased levels of serum Ig. Some forms of lupus autoimmunity are severely reduced. (Christianson, J Immunol 156:4932-9, 1996). Hemachromatosis has been noted in certain genetic backgrounds (Rothenberg BE, Voland JR, Proc Natl Acad Sci USA 93:1529-34, 1996). The B2mtm1Un mutation backcrossed to the NOD/Lt strain serves as a MHC class I-negative, CD8+ deficient diabetes resistant stock
..... For more information please see the full phenotype on the strain data sheet | ||
| 004222 | NOD.129P2(B6)-Il4tm1Cgn/DvsJ | Repository-Cryopreserved |
| Complete Freund's adjuvant (CFA) induced suppression of diabetes in NOD mice has been associated with a shift to Th2 cytokine production. NOD mice deficient in IL4 were created to investigate the role of IL4 in this shift. Mice homozygous for the Il4tm1Cgn targeted mutation are viable and fertile. T and B cell development is normal but IgG1and IgE levels and the ability of homozygous mutant mice to produce Th2-derived cytokines are significantly reduced. IL4 deficient NOD mice develop IDDM with the same incidence as standard NOD/Lt controls, and there is no change between IL4 deficient and wildtype NOD in disease protection conferred by treatment of bacillus Calmette-Guerin vaccine (BCG) or CFA. Both IL4 deficient and wildtype NOD mice are significantly protected from insulitis by treatment of CFA but not by treatment of BCG. (Serreze et al 2001) | ||
| 004444 | NOD.129P2(C)-Tcratm1Mjo/DoiJ | Repository-Cryopreserved |
| NOD mice homozygous for the Tcratm1Mjo targeted mutation lack alpha beta T cells, and therefore, are completely protected from diabetes development. Because of the complete elimination of alpha beta T cells, these mice are useful in adoptive transfer experiments (as in Hoglund et al. 1999). | ||
| 004448 | NOD.129S2(B6)-Ciitatm1Ccum/FlvJ | Repository-Cryopreserved |
| In humans, a non-functional C2ta (or Ciita) gene causes bare lymphocyte syndrome (BLS), which is characterized by the lack of HLA class II gene expression and a reduced number of mature CD4+ T cells in the periphery. On the C57BL/6 congenic background (see Stock No. 003239) disruption of C2ta results in a lack of MHC Class II expression by splenic B cells, dendridic cells, and both resting and interferon gamma stimulated macrophages. However, thymic epithelium retains MHC class II expression. Homozygotes also exhibit a significant decrease in the levels of invariant chain and H-2M gene transcripts. Non-conventional MHC Class II molecules such as H-2O alpha and H-2O beta, are not affected by the disruption of C2ta. Despite the continued expression of MHC Class II molecules on cells of the thymic epithilium, few CD4 positive cells exist in the periphery of homozygotes. (Chang et al 1996) Because of
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| 005035 | NOD.129S2(B6)-Ins1tm1Jja/GseJ | Repository-Cryopreserved |
| Ins1tm1Jja homozygotes are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. There is no detectable expression of Ins1 in the pancreas by RT-PCR and similar levels of insulin auto-antibodies develop in NOD.129S2(B6)-Ins1tm1Jja homozygotes as are found in NOD controls. However, neither homozygous nor heterozygous males develop diabetes, compared with >20% of wild-type littermates, and less than 5% of the Ins1tm1Jja homozygous females and 40% of the heterozygous females become diabetic compared with >80% of wild-type females when followed for 1 year. Histological evaluation found 48 week old homozygous and heterozygous males to have either minimal periinsulitis or no insulitis. Heterozygous females had more extensive insulitis than heterozygous males and homozygous females had minimal intra-ductal infiltrates and no insulitis, whereas wild type littermates had severe insul
..... For more information please see the full phenotype on the strain data sheet | ||
| 004672 | NOD.129S2(Cg)-Stat6tm1Gru/JbsJ | Repository-Cryopreserved |
| NOD mice homozygous for the Stat6tm1Gru mutation exhibit an increased diabetes incidence compared to NOD controls and show a striking defect in the generation of Th2 cells. Lymphocytes are unable to respond to IL4 as measured in a variety of in vitro and in vivo assays. This strain can be used to look at the role of Il4 in diabetes development. | ||
| 002575 | NOD.129S7(B6)-Ifngtm1Ts/DvsJ | Repository-Cryopreserved |
| Mice homozygous for the Ifngtm1Ts targeted mutation are viable and fertile. This Ifng -deficient mutant develops type 1 diabetes at the same rate as the NOD/ShiLt parental strain. | ||
| 005073 | NOD.ABH-(D18Mit19-D18Mit4)/TrmJ | Repository-Cryopreserved |
| NOD.ABH-(D18Mit19-D18Mit4)/TrmJ, commonly referred to as NOD. Chr18ABH, has a significantly decreased diabetes rate (34%by 30 weeks of age) when compared to wild-type or NOD controls (approximately 80-85% by 30 weeks of age). This strain is useful for dissecting the role of non-MHC susceptibility genes in autoimmune diabetes. | ||
| 004309 | NOD.ALR-(D17Mit16-D17Mit10)/LtJ | Repository-Cryopreserved |
| This allelic congenic strain commonly called D.R1, carries a defined segment of Chr. 17 that includes the ALR H2gx complex and insulin dependent diabetes susceptibility locus 16, Idd16aALR. At 35 weeks of age diabetes incidence in this NOD.ALR strain is significantly suppressed with about 60% of the females and less than 20% of the males diabetic as compared to NOD/ShiLt in which 100% of the females and nearly 70% of the males were diabetic. Histological exam of the pancreas of 40-week old pre-diabetic animals showed widespread intra-islet insulitis. This strain is useful for identifying candidate genes and dissecting the role of Idd16a in autoimmune diabetes. | ||
| 004308 | NOD.ALR-(D17Mit16-H2-D)/LtJ | Repository-Cryopreserved |
| This allelic congenic strain commonly called D.R2, carries a defined segment of Chr 17 that includes the ALR H2gx complex and insulin dependent diabetes susceptibility locus 16, Idd16aALR. At 35 weeks of age diabetes incidence in this NOD.ALR strain is significantly suppressed with 50% of the females and almost 15% the males diabetic as compared to NOD/ShiLt in which 100% of the females and nearly 70% of the males were diabetic. Similar to Stock No. 004309 pancreatic histological examination of pre-diabetic 8-week old males show lower mean insulitis scores than controls. This strain is useful for identifying candidate genes and dissecting the role of Idd16a in autoimmune diabetes. | ||
| 005311 | NOD.B6-(D1Mit18-D1Mit445)(D11Nds1-D11Mit41)/DelJ | Repository-Cryopreserved |
The donating investigator reports diabetes onset of female NOD.B6-(D1Mit18-D1Mit445) (D11Nds1-D11Mit41)/DelJ (commonly called NOD.B6-Idd4A, Chr 11, 43.8-49cM) is delayed, with 15% of the females and 5% of the males becoming diabetic by 30 weeks of age. In the same colony, diabetes rates in NOD controls are 75% in females and 45% in males by 30 weeks of age. Histological examination of 12-week-old NOD.B6-Idd4A mice indicates 70% of the islets are normal compared with 50% in NOD controls. At 25-30 weeks of age, 10% of NOD.B6-Idd4A islets are infiltrated compared to 80% in NOD controls. Until 25-30 weeks of age, NOD.B6-Idd4A mice only develop periductal infiltrates with mild non-destructive insulitis. Additionally, immunohistochemical assays indicate normal amounts of stored insulin. Purified splenic T-cells from 12-week-old, non-diabetic NOD.B6-Idd4A females alone are able to induce diabetes in NOD.Prkdcscid female rec
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| 005313 | NOD.B6-(D1Mit180-D1Mit143)(D11Mit38-D11Mit41)/DelJ | Repository-Cryopreserved |
| The donating investigator reports diabetes onset of female NOD.B6-(D11Mit38-D11Mit41)/DelJ (commonly called NOD.B6-Idd4C, Chr 11, 49cM) is delayed, with 20% of the females becoming diabetic by 30 weeks of age. In the same colony, diabetes rates in NOD controls are 75% in females and 45% in males by 30 weeks of age. Histological examination of 12-week-old NOD.B6-Idd4C mice indicates 70% of the islets are normal compared with 50% in NOD controls. At 25-30 weeks of age, 45% of NOD.B6-Idd4C islets are infiltrated compared to 80% in NOD controls. Immunohistochemical assays indicate normal amounts of stored insulin. Purified splenic T-cells from 12-week-old, non-diabetic NOD.B6-Idd4C females alone are able to induce diabetes in NOD.Prkdcscid female recipients. Diabetes onset is delayed in recipients of NOD.B6-Idd4C T-cells only, with about 40% becoming diabetic by 70 days post transfer compared to 80% diabetic in recipients receivin
..... For more information please see the full phenotype on the strain data sheet | ||
| 005312 | NOD.B6-(D1Mit18-D1Jmp12)(D11Mit325-D11Mit41)/DelJ | Repository-Cryopreserved |
| The donating investigator reports diabetes onset of female NOD.B6-(D11Mit38-D11Mit325)/DelJ (commonly called NOD.B6-Idd4B, Chr 11, 49cM) is delayed, with 40% of the females becoming diabetic by 30 weeks of age. In the same colony, diabetes rates in NOD controls are 75% in females and 45% in males by 30 weeks of age. Histological examination of 12-week-old NOD.B6-Idd4B mice indicates 70% of the islets are normal compared with 50% in NOD controls. At 25-30 weeks of age, 45% of NOD.B6-Idd4B islets are infiltrated compared to 80% in NOD controls. Immunohistochemical assays indicate normal amounts of stored insulin. Purified splenic T-cells from 12-week-old, non-diabetic NOD.B6-Idd4B females alone are able to induce diabetes in NOD.Prkdcscid female recipients. Diabetes onset is delayed in recipients of NOD.B6-Idd4B T-cells only, with about 50% becoming diabetic by 70 days post transfer compared to 80% diabetic in recipients rec
..... For more information please see the full phenotype on the strain data sheet | ||
| 007573 | NOD.B6-(D6Mit254-D6Mit289)/CarJ | Repository-Cryopreserved |
| Klrb1ca (Nk1.1) homozygous mice are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. Nk1.1 expression in the strain has been confirmed by FACS analysis of peripheral blood cells. The C57BL/6-derived congenic interval on Chromosome 6 which contains the Nk1.1 locus is shorter in these mice than that carried in the original strain (Stock No. 004482). Diabetes incidence in this strain is higher than that reported in strain 004482 (65% in females and 15% in males by 27 weeks for this strain versus 30% in the females and 0% males by 30 weeks of age for Stock No. 004482). Histological examination of the pancreas from 27-week old, non-diabetic mice reveals extensive insulitis that is not significantly different from that seen in similarly
..... For more information please see the full phenotype on the strain data sheet | ||
| 004482 | NOD.B6-(D6Mit254-D6Mit339)/CarJ | Repository-Cryopreserved |
| Klrb1ca homozygous mice are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. Diabetes incidence as reported by donating investigator and confirmed in the T1DR, prior to shortening the congenic interval, is significantly decreased (30% females and 0% males at 30 weeks of age) as compared to standard NOD (NK1.2) controls (85% females and 60% males at 30 weeks of age) . FACS analysis of NKT cells derived from thymus or spleen of NOD animals homozygous for this genomic segment revealed the presence of NK1.1+/TCR alpha beta +, V beta8+ and CD44+, but at lower levels than in C57BL/6 controls. NK cells of NOD.B6-(D6Mit254-D6Mit14) exhibit an equivalent number of NK1.1/DX5 double positive cells when compared to C57BL/6. Histological examination of 10-12 week old animals indicates no significant difference in insulitis severity between NOD.B6-(D6Mit254-D6Mit14) and NOD control islets (Carnaud et al, 2001). Confir
..... For more information please see the full phenotype on the strain data sheet | ||
| 003585 | NOD.B6-(Gpi1-D7Mit346)/LtJ | Repository-Cryopreserved |
| NOD.B6-(Gpi1-D7Mit346)/LtJ mice are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. Congenic NOD Gpib mice become diabetic at a similar rate and onset as NOD/Lt (Chen et al, 2005). Gpi1b in these mice can be used as a marker for transplant studies. | ||
| 003505 | NOD.B6-Prf1tm1Sdz/J | Repository-Cryopreserved |
| Mice homozygous for the Prf1tm1Sdz targeted mutation are viable and fertile. Homozygous mutant mice on an autoimmune type 1 diabetes prone NOD background have normal numbers of CD4- CD8+ T cells in the spleen. CD4- CD8- expressing T lymphocytes were also normal. NOD mice show a progressive infilitatraion of mononuclear cells into pancreatic islets beginning around 5 weeks of age. NOD wildtype and PRF1 deficient mice show similar development of insulititis. However, disease incidence was decreased from 77% in wildtype females to 16% in homozygotes. The onset of disease was also delayed from a median of 19 weeks to 39.5 weeks of age. These results show the importance of perforin-mediated cytotoxic T cells in development of autoimmune diabetes. (Kagi et al., 1994; Kagi et al., 1997.) | ||
| 005512 | NOD.B6-Tg(HLA-A2.1)1Enge/DvsJ | Repository-Cryopreserved |
| Homozygous mice carrying the (HLA-A2.1)1Enge transgene ubiquitously express significant quantities of the human MHC class I HLA-A2.1 molecules. These HLA-A2.1 molecules mediate beta cell auto-reactive CD8 T cell responses that when added to those elicited by endogenous murine MHC class I variants results in a significantly accelerated rate of diabetes onset in either the hemizygote or homozygote transgenic mouse when compared to NOD/Lt controls (Marron et al., 2002). This model is useful for studying the role of MHC class I molecules in Type 1 Diabetes. | ||
| 006345 | NOD.B6-Tg(IghelMD4)4Ccg/DvsJ | Repository-Cryopreserved |
| NOD.B6-Tg(IghelMD4)4Ccg/DvsJ (commonly referred to as NOD.IgHEL) mice are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. The transgene encodes IgM and IgD molecules specific for the pancreatic beta cell-irrelevant Hen Egg Lysozyme (HEL) protein. NOD transgenic mice have a 2-fold increase in the total numbers of splenic B-lymphocytes when compared to NOD wildtype mice, a value that is comparable to that seen in B6 mice. The total number of CD4+ and CD8+ T-lymphocytes did not differ significantly between NOD transgenic and NOD wildtype mice. Ninety-nine percent of splenic B-lymphocytes express the transgenic IgMa; however 8% of the B-lymphocytes from transgenic mice escaped allelic exclusion, and express endogenous IgMb molecules. Diabetes onset in NOD.IgHEL females is significantly delayed, although the final incidence at 30 weeks of age did not differ significan
..... For more information please see the full phenotype on the strain data sheet | ||
| 006610 | NOD.B6-Tg(ML5sHEL)5Ccg/DvsJ | Repository-Cryopreserved |
| Transgenic mice are viable, fertile, normal in size, agouti in color and express a soluable form of hen egg lysozyme. They become diabetic at a rate similar to NOD controls. This strain can be used to study B-cell selection and tolerance as it relates to Type 1 Diabetes. | ||
| 005616 | NOD.C-(Ptprc-D1Mit262)/WehiJ | Repository-Cryopreserved |
| This NOD/LtJWehi congenic strain is carrying Chr 1alleles derived from BALB/cWehi including Ptprcb. Diabetes onset and incidence is similar between NOD.C-(Ptprc-D1Mit262)/WehiJ congenic mice (6/8 by 300 days of age) and NOD/LtJWehi (17/24 by 300 days of age). NOD.C-(Ptprc-D1Mit262)/WehiJ bone marrow transplanted into irradiated NOD/LtJWehi recipients yielded incomplete replacement of donor leukocytes at 16 weeks post transfer versus nearly complete replacement of donor leucocytes in C57BL/6Wehi and B6.SJL/Wehi irradiated mice (Steptoe, et al., 2004, Journal of AutoImmunity, Vol 22, p131-138). This strain provides a unique cell surface marker that can be used to track lineage and phenotype of all hematopoietic donor derived or transferred cells making it useful in studies monitoring diabetes progression. | ||
| 004306 | NOD.CBALs-Hc1/LtJ | Repository-Cryopreserved |
| This NOD/Lt congenic strain is carrying Chr 2 alleles derived from CBA/Ls including Hc1. Diabetes onset and incidence is the same as NOD/Lt. | ||
| 004304 | NOD.CBALs-Tyr+/LtJ | Repository-Cryopreserved |
| This Chr 7 congenic strain in which the tyrosinase allele Tyr+ of the CBA/JLsLt strain is fixed on the NOD/Lt background, therefore making the strain agouti in color. This strain should be a good donor for blastocysts in which to microinject targeted NOD ES cells, and may alleviate unwanted genome integration experienced with use of the C57BL/6 blastocysts. The congenic segment on Chr 7 slightly supresses spontaneous T1D development which is an asset when these females are used as blastocyst recipients. | ||
| 005345 | NOD.Cg-Cd38tm1Lnd Prkdcscid/LtJ | Repository-Cryopreserved |
| CD38 is an ADP-ribosyl cyclase/cyclic ADP-ribose hydrolase. This ubiquitously expressed ectoenzyme is the major NAD hydrolase in mice. NOD/Lt mice homozygous for the Cd38tm1Lnd targeted allele develop accelerated Type 1 diabetes associated with an ART2 (T cell ADP-ribosyltransferase)-dependent and NAD-mediated loss of regulatory CD4+CD25+ Foxp3+ and CD4+iNKT cells (Chen, J. et al 2006; Chen, Y.G et al 2006). Combining the Prkdcscid mutation with the Cd38tm1Lnd targeted allele completely prevents diabetes development. For investigators wishing to study the role of CD38 in beta cell biology, the presence of the Prkdcscid allele provides insultis-free islets for analysis. Congenic, doubly homozygous NOD.Cd38tm1Lnd Prkdcscid mutant mice exhibit no significant difference in glucose tolerance when compared to NOD or NOD. Prkdcscid, thus not suppor
..... For more information please see the full phenotype on the strain data sheet | ||
| 006021 | NOD.Cg-H2-Ab1tm1Gru Tg(CD2-CD4,HLA-DQA1,HLA-DQB1)1Ell/EllJ | Repository-Cryopreserved |
| The NOD transgenic HLA DQ8, H2-Ab1deficient mouse is diabetes resistant but develops cardiomyopathy resulting in early death from heart failure in both males and females. Histological exam indicates hearts are 3-4x larger than wildtype. Pathology results from an autoimmune response against normal cardiomyocytes in the atrial and ventricular walls, as well as against myocytes present in the outermost muscle layer surrounding the pulmonary veins. Disease progression can be blocked by cyclosporin A treatment and is accelerated with Complete Freund’s Adjuvant (Elliott et al, 2003, PNAS) . This model is useful for studying autoimmune myocarditis, idiopathic dilated cardiomyopathy and heart failure and to understand the role of MHC class II in autoimmunity.. | ||
| 004447 | NOD.Cg-H2h4/DilTacUmmJ | Repository-Cryopreserved |
| NOD.Cg-H2h4/DilTacUmm mice are completely protected from diabetes; however, a low incidence of perivascular and periductal insulitis is detected (20-30%). Protection from diabetes is complete even upon treatment with cyclophosphamide. These mice do, however, develop spontaneous thyroiditis and produce IgG autoantibodies when treated with 0.05% NaI in water (100% incidence in both sexes 6-8 week post treatment or by 4 months of age). Without treatment, thyroiditis is delayed and incomplete (60-70% incidence in 7-10 month old mice). This strain is an excellent model for autoimmune thyroiditis. | ||
| 005346 | NOD.Cg-Il10tm1Cgn Casp1tm1Sesh/LtJ | Repository-Cryopreserved |
| Mice homozygous for the Il10 and Casp1 targeted mutations are viable and fertile when housed under SPF conditions. NOD/Lt mice deficient for both of these genes develop type 1 diabetes at a rate equivalent to the parental strains. The Il10 targeted mutation also renders this NOD/Lt stock susceptible to colitis (although not as severe as other strains of Il10 deficient mice) when maintained under standard housing conditions. | ||
| 004291 | NOD.Cg-Il10tm1Cgn Il4tm1Cgn/DvsJ | Repository-Cryopreserved |
| Mice homozygous for the Il10 and Il4 targeted mutations are viable and fertile when housed under SPF conditions. NOD/Lt mice deficient for both of these genes develop type 1 diabetes at a rate equivalent to the parental strain. The Il10 tm1Cgn mutation also renders this NOD/Lt stock susceptible to colitis (although not as severe as other strains of Il10 deficient mice) when maintained under standard housing conditions. | ||
| 004266 | NOD.Cg-Il10tm1Cgn/DvsJ | Repository-Cryopreserved |
| Mice homozygous for the Il10tm1Cgn targeted mutation are viable and fertile when housed under SPF conditions. This mutant develops type 1 diabetes at the same rate as the NOD/Lt parental strain. The Il10 tm1Cgn mutation also renders this NOD/Lt stock susceptible to colitis (although not as severe as other strains of Il10 deficient mice) when maintained under standard housing conditions. | ||
| 005078 | NOD.Cg-Il1r1tm1Roml/HetJ | Repository-Cryopreserved |
| Mice homozygous for the Il1r1tm1Roml targeted mutation develop normally, exhibit a reduced inflammatory response and no response to interleukin-1 alpha or beta. Homozygous mice have a reduced acute phase and delayed type hypersensitivity response and are highly susceptible to Listeria monocytogenes infection. Equilibrium binding experiments using radiolabeled anti-mouse IL1R1 antibody, 35F5, show no detectable expression of IL1R1 protein in primary murine embryonic fibroblasts (Labow et al, 1997). NOD females homozygous for the Il1r1tm1Roml mutation experience a slight, yet significant delay in diabetes development, with an overall incidence of 75% compared to 100% in wild types. There is no statistical difference between mutant and wild type NOD mice in diabetes development following cyclophosphamide treatment or in the rate at which they mediate autoimmune rejection of syngeneic fetal pancreatic grafts. Adoptive transfer of NOD.Cg-Tg(TcraBDC
..... For more information please see the full phenotype on the strain data sheet | ||
| 006698 | NOD.Cg-Il4tm1Lky/JbsJ | Repository-Cryopreserved |
| A "knock-in" replaces the endogenous gene with an Il4/IRES/EGFP bicistronic construct, which places both IL4 and EGFP expression under the control of the endogenous Il4 gene regulatory elements. IL4 activity in these mutant mice remains intact. Cells activated to express IL4 also express EGFP allowing reliable in vivo tracking of both innate and adaptive immune cells and enabling their isolation without further stimulation. Because the IRES element promotes translational competence capable of revealing low-level transcription otherwise not apparent from the canonical 5'-cap of the mRNA, cells from these mice also can be used to report competence for IL4 production upon stimulation. This knock-in allele has been backcrossed to NOD for 15 generations. Diabetes incidence in mutant mice is reported to be about 60%, which is not statistically different from wild-type cohorts or NOD inbred mice. | ||
| 006609 | NOD.Cg-Prkdcscid Tg(HLA-A2.1)1Enge/DvsJ | Repository-Cryopreserved |
| Although transgenic NOD mice develop diabetes significantly earlier than do NOD/ShiLtDvs (NOD) mice, this transgenic strain harbors the Prkdcscid mutation (characterized by an absence of functional T cells and B cells) and therefore does not become diabetic. This strain is useful for adoptive transfer experiments and as a source of insulitis free pancreatic islets. | ||
| 004346 | NOD.Cg-Prkdcscid Tg(Ins2-CD80)3B7Flv/DvsJ | Repository-Cryopreserved |
| These mice are characterized by pancreatic beta cells that express a rat insulin promoter (Rip) regulated transgene encoding the human CD80 T cell co-stimulatory molecule. They are an excellent source of MHC class I positive, CD80 transgene-expressing islet cells, a potent antigenic reagent for propagating diabetogenic CD8+ T lymphocytes derived from NOD mice in vitro. The presence of the Prkdcscid allele eliminates the possibility that isolated islet cells will introduce contaminating T lymphocytes onto cultures. | ||
| 004606 | NOD.Cg-Prkdcscid H2-Ab1tm1Doi Tg(HLA-DQA1,HLA-DQB1)1Dv/SzJ | Repository-Cryopreserved |
| This strain which is MHC II deficient and has no functional T or B cells expresses a humanized transgenic HLA-DQ8 molecule that has been linked to IDDM development. This model is a valuable genetic tool for identifying the role of HLA-DQ8 in Type 1 Diabetes. | ||
| 004347 | NOD.Cg-Rag1tm1Mom Tg(TcraAI4)1Dvs/DvsJ | Repository-Cryopreserved |
| The rearranged Tcra transgene expressed in these mice is derived from the pancreatic beta cell-reactive CD8 T lymphocyte clone AI4. The presence of the nonfunctional Rag1tm1Mom allele renders mice incapable of rearranging endogenous T cell receptor genes. When crossed with strain NOD.Cg-Tg(TcrbAI4)1DvsRag1tm1Mom/DvsJ (004348), the resulting animals that carry both the alpha and beta AI4 TCR transgenes exhibit an accelerated development of insulin-dependent diabetes mellitus (IDDM). Additionally, transgenic animals bearing both TCR transgenes offer a source of CTL precursors useful in examining the diversity of beta cell peptides recognized by the autoreactive CD8+ T lymphocytes contributing to the earliest phase of IDDM development. Homozygous mice are viable and fertile. | ||
| 004348 | NOD.Cg-Rag1tm1Mom Tg(TcrbAI4)1Dvs/DvsJ | Repository-Cryopreserved |
| The rearranged Tcrb transgene expressed in these mice is derived from the pancreatic beta cell-reactive CD8 T lymphocyte clone AI4. The presence of the nonfunctional Rag1tm1Mom allele renders mice incapable of rearranging endogenous T cell receptor genes. When crossed with strain NOD.Cg-Tg(TcraAI4)1Dvs-Rag1tm1Mom/DvsJ (004347), the resulting animals that carry both the alpha and beta AI4 TCR transgenes exhibit an accelerated development of insulin-dependent diabetes mellitus (IDDM). Additionally, transgenic animals bearing both TCR transgenes offer a source of CTL precursors useful in examining the diversity of beta cell peptides recognized by the autoreactive CD8+ T lymphocytes contributing to the earliest phase of IDDM development. Homozygous mice are viable and fertile. | ||
| 006024 | NOD.Cg-Rag1tm1Mom H2-Ab1tm1Gru Tg(CD4,HLA-DQA1,HLA-DQB1)N8Ell/EllJ | Repository-Cryopreserved |
| Rag1 and H2-Ab1 deficient NOD mice carrying transgenes encoding humanized CD4 and HLA-DQ6 lack T and B cells and are free of autoimmune diabetes and cardiomyopathy, and do not develop thyroiditis. This model is useful in adoptive transfer experiments and in studying MHC class II-based resistance and susceptibility in autoimmunity. | ||
| 006022 | NOD.Cg-Rag1tm1Mom H2-Ab1tm1Gru Tg(CD2-CD4,HLA-DQA1,HLA-DQB1)1Ell/EllJ | Repository-Cryopreserved |
| Rag1 and H2-Ab1 deficient NOD mice carrying transgenes coding for human CD2-CD4 and HLA-DQ8 lack T and B cells, and are diabetes free. Also, unlike the H2-Ab1 deficient, transgenic CD4, HLA-DQ8 mice (see Stock No. 006621), this strain does not develop cardiomyopathy. This model is useful in adoptive transfer experiments and to understand the role of MHC class II in autoimmunity. | ||
| 005853 | NOD.Cg-Tg(HLA-A2/H2-K)1Scr/ShrmJ | Repository-Cryopreserved |
| Transgenic mice are viable, fertile, normal in size and do not display any behavioral abnormalities. FACs analysis indicates expression of HLA-A201 on peripheral blood lymphocytes. The level of expression of this chimeric MHC I molecule in transgenic mice is similar to the observed expression in human PBL's. Diabetes incidence of mice carrying this transgene (88%) is similar to NOD (79%) at 25 weeks of age. Splenocytes from transgenic mice immunized with GAD65 peptides together with MHC class II helper peptide were re-stimulated with peptide pulsed irradiated syngeneic APC?s in-vitro 10 days post immunization Transgenic mice immunized with three different GAD65 peptides (position: 144-149, sequence: LLQEYNWEL; position: 114-122, sequence: VMNILLQYV; and position 573-581, sequence: FLIEEIERL) gave vigorous CTL responses when tested by standard chromium release assays. FACs analysis indicates presence of CFSE expression on CD8+ T-cells in transgenic mice given CFSE-labeled
..... For more information please see the full phenotype on the strain data sheet | ||
| 005019 | NOD.Cg-Tg(Igh-6/Igh-V125)2Jwt/JwtJ | Repository-Cryopreserved |
| 005018 | NOD.Cg-Tg(Igk-C/Igk-V125)1Jwt/JwtJ | Repository-Cryopreserved |
| 005524 | NOD.Cg-Tg(Ins2*Y16A)1Ell Ins1tm1Jja Ins2tm1Jja/GseJ | Repository-Cryopreserved |
| Transgenic mice reportedly express the mutant Ins2*Y16A protein in the pancreatic islets and thymus. The donating investigator reports approximately 75% of female transgenic mice (founder line B) become diabetic in the presence of native insulin genes by 35 weeks of age. In contrast, NOD female transgenic mice lacking both Ins1 and Ins2 fail to produce insulin autoantibodies, and neither diabetes nor insulitis develops by 26 weeks of age. Sialitis does occur, however. Line B transgenics have lower expression levels than line F (see Stock No. 005525), and 50% of the line B male transgenics lacking both Ins1 and Ins2 develop metabolic diabetes, with little to no insulitis, before 10 weeks of age. This strain is useful to study insulin-reactive autoimmunity. | ||
| 005525 | NOD.Cg-Tg(Ins2*Y16A)3Ell Ins1tm1Jja Ins2tm1Jja/GseJ | Repository-Cryopreserved |
| Expression has been reported in the pancreatic islets and thymus of NOD mice carrying the Tg(Ins2*Y16A)3Ell mutation. Approximately 15% of line F female transgenic mice become diabetic in the presence of native insulin genes by 35 weeks of age. NOD female transgeni | ||