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- Description
- Phenotype
- Genes & alleles
- Genotyping
- Health & husbandry
- References
- Purchasing information
- Terms of Use
Description
Strain Information
Type Congenic; Major Histocompatibility Congenic; Mutant Strain; Additional information on Genetically Engineered Mutant Mice. Species laboratory mouse Background Strain NOD/MrkTac Donor Strain B10.A-H2h4/(4R)SgDvEg H2 Haplotype h4 Generation N5F?+F1p Appearance
albino, pink-eyed
Related Genotype: A/A Tyrc/TyrcDescription
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.Development
NOD/MrkTac were outbred to B10.A-H2h4/(4R)SgDvEg (Stock# 001150), which carries the recombinant major histocompatibility H2h4 haplotype. The offspring were then backcrossed to NOD/MrkTac for five generations selecting for H2h4 at each generation. At N6, individuals heterozygous for the H2h4 MHC were intercrossed and resulting homozygous individuals were brother-sister mated.
Control Information
| Control | ||
|---|---|---|
| 001976 NOD/ShiLtJ | ||
| Considerations for Choosing Controls | ||
Related Strains
Strains carrying H2h4 allele
001150 B10.A-H2h4/(4R)SgDvEgJ View Strains carrying H2h4 (1 strain)
Additional Web Information
Congenic Nomenclature
Phenotype
Phenotype Information
assigned by genotype
H2h4/H2h4
NOD.Cg-H2h4
- homeostasis/metabolism phenotype
- decreased sensitivity to xenobiotics (MGI Ref ID J:14178)
- no female mice homozygous for this haplotype develop diabetes after cyclophosphamide injections
- endocrine/exocrine gland phenotype
- insulitis (MGI Ref ID J:14178)
- female mice develop insulitis between 8 and 10 months of age
- periinsulitis (MGI Ref ID J:14178)
- female mice display spontaneous perivascular and periductal lymphocytic infiltration by 8-10 months of age; mice between 5 and 13 months of age that are treated with cyclophospamide display perivascular and periductal infiltrates
- thyroid inflammation (MGI Ref ID J:54563)
- almost 100% of mice develop thyroiditis 6-8 weeks after receiving NaI in water beginning at 8 weeks of age; lesions are observed as early as 2 weeks after the start of NaI supplementation
- without NaI supplementation, many H2h4 mice develop lesions, but lesions are rarely observed before 6 months of age
- lesion severity peaks at about 8 weeks and remains unchanged until 23 weeks; response is chronic if NaI treatment is stopped after 7 weeks
- males develop more severe lesions more frequently than females
- with CD4+ T cell depletion prior to autoantibody production, mice do not develop SAT; depletion of CD8+ T cells has little effect on severity of lesions
- immune system phenotype
- abnormal cytokine secretion (MGI Ref ID J:54563)
- mice which do not have thyroiditis express barely detectable levels of cytokines (Ifng, Il4, 5, 10, 13 and Tnfa); with development of lesions about 4-6 weeks after start of NaI treatment, expression of all cytokines except Tgfb increases
- decreased susceptibility to autoimmune diabetes (MGI Ref ID J:14178)
- no female mice homozygous for the haplotype develop diabetes spontaneously
- insulitis (MGI Ref ID J:14178)
- female mice develop insulitis between 8 and 10 months of age
- periinsulitis (MGI Ref ID J:14178)
- female mice display spontaneous perivascular and periductal lymphocytic infiltration by 8-10 months of age; mice between 5 and 13 months of age that are treated with cyclophospamide display perivascular and periductal infiltrates
- thyroid inflammation (MGI Ref ID J:54563)
- almost 100% of mice develop thyroiditis 6-8 weeks after receiving NaI in water beginning at 8 weeks of age; lesions are observed as early as 2 weeks after the start of NaI supplementation
- without NaI supplementation, many H2h4 mice develop lesions, but lesions are rarely observed before 6 months of age
- lesion severity peaks at about 8 weeks and remains unchanged until 23 weeks; response is chronic if NaI treatment is stopped after 7 weeks
- males develop more severe lesions more frequently than females
- with CD4+ T cell depletion prior to autoantibody production, mice do not develop SAT; depletion of CD8+ T cells has little effect on severity of lesions
- digestive/alimentary phenotype
- insulitis (MGI Ref ID J:14178)
- female mice develop insulitis between 8 and 10 months of age
- periinsulitis (MGI Ref ID J:14178)
- female mice display spontaneous perivascular and periductal lymphocytic infiltration by 8-10 months of age; mice between 5 and 13 months of age that are treated with cyclophospamide display perivascular and periductal infiltrates
This mouse can be used to support research in many areas including:
Diabetes and Obesity Research
Type 1 Diabetes (IDDM) Analysis Strains (NOD/ShiLtJ MHC Congenics)
Immunology and Inflammation Research
CD Antigens, Antigen Receptors, and Histocompatibility Markers
Inflammation
Genes & Alleles
Gene & Allele Information
| Allele Symbol | H2h4 | ||
|---|---|---|---|
| Allele Name | h4 variant | ||
| Allele Type | Not Applicable | ||
| Common Name(s) | H-2h4; | ||
| Gene Symbol and Name | H2, histocompatibility-2, MHC | ||
| Chromosome | 17 | ||
| Gene Common Name(s) | H-2; MHC-II; | ||
| General Note | This variant has been observed in the following strains: B10.A(4R) | ||
Genotyping
Genotyping Information
This strain will not have a genotyping protocol or one is not currently available.
Helpful Links
Optimizing PCR Protocols
References
References
Selected Reference(s)
Podolin PL; Pressey A; DeLarato NH; Fischer PA; Peterson LB; Wicker LS. 1993. I-E+ nonobese diabetic mice develop insulitis and diabetes. J Exp Med 178(3):793-803. [PubMed: 8350054] [MGI Ref ID J:14178]
Additional References
Braley-Mullen H; Sharp GC; Medling B; Tang H. 1999. Spontaneous autoimmune thyroiditis in NOD.H-2h4 mice. J Autoimmun 12(3):157-65. [PubMed: 10222025] [MGI Ref ID J:54563]
H2h4 relatedBraley-Mullen H; Sharp GC; Medling B; Tang H. 1999. Spontaneous autoimmune thyroiditis in NOD.H-2h4 mice. J Autoimmun 12(3):157-65. [PubMed: 10222025] [MGI Ref ID J:54563]
Braley-Mullen H; Yu S. 2000. Early requirement for B cells for development of spontaneous autoimmune thyroiditis in NOD.H-2h4 mice J Immunol 165(12):7262-9. [PubMed: 11120860] [MGI Ref ID J:66106]
Fang Y; Sharp GC; Braley-Mullen H. 2008. Interleukin-10 promotes resolution of granulomatous experimental autoimmune thyroiditis. Am J Pathol 172(6):1591-602. [PubMed: 18467701] [MGI Ref ID J:136188]
Hutchings PR; Verma S; Phillips JM; Harach SZ; Howlett S; Cooke A. 1999. Both CD4(+) T cells and CD8(+) T cells are required for iodine accelerated thyroiditis in NOD mice. Cell Immunol 192(2):113-21. [PubMed: 10087179] [MGI Ref ID J:54320]
Levisetti MG; Lewis DM; Suri A; Unanue ER. 2008. Weak proinsulin peptide-major histocompatibility complexes are targeted in autoimmune diabetes in mice. Diabetes 57(7):1852-60. [PubMed: 18398138] [MGI Ref ID J:138230]
Miyashita N; Migita S; Moriwaki K. 1987. Effects of H-2 complex and non-H-2 background on urethane-induced chromosomal aberrations in mice. Mutat Res 176(1):59-67. [PubMed: 3099189] [MGI Ref ID J:109945]
Nagayama Y; Horie I; Saitoh O; Nakahara M; Abiru N. 2007. CD4(+)CD25(+) naturally occurring regulatory T cells and not lymphopenia play a role in the pathogenesis of iodide-induced autoimmune thyroiditis in NOD-H2(h4) mice. J Autoimmun 29(2-3):195-202. [PubMed: 17826032] [MGI Ref ID J:125178]
Sharma R; Traore K; Trush MA; Rose NR; Burek CL. 2008. Intracellular adhesion molecule-1 up-regulation on thyrocytes by iodine of non-obese diabetic.H2(h4) mice is reactive oxygen species-dependent. Clin Exp Immunol 152(1):13-20. [PubMed: 18241232] [MGI Ref ID J:133583]
Yu S; Sharp GC; Braley-Mullen H. 2008. TGF-beta promotes thyroid epithelial cell hyperplasia and fibrosis in IFN-gamma-deficient NOD.H-2h4 mice. J Immunol 181(3):2238-45. [PubMed: 18641364] [MGI Ref ID J:139224]
Health & husbandry
Health & Colony Maintenance Information
Currently there no information available for this strain. This may be due to the supply level of this strain.
Purchasing information
Pricing, Supply Level & Notes, Controls, General Terms & Conditions
Pricing
| Pricing for USA, Canada and Mexico shipping destinations |
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*Price(s) in US dollars ($)
Weeks of Age Price* Gender Cryorecovery Fee $1900.00
Additional Supply Details
| Pricing for International shipping destinations |
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*Price(s) in US dollars ($)
Weeks of Age Price* Gender Cryorecovery Fee $2470.00
Additional Supply Details
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Supply Details
| Standard Supply | Repository-Cryopreserved. Must Be Recovered. Please refer to pricing and supply notes for further information. |
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| Supply Notes |
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Control Information
| Control | ||
|---|---|---|
| 001976 NOD/ShiLtJ | ||
| Considerations for Choosing Controls | ||
| USA, Canada and Mexico - Control Pricing Information for Genetically Engineered Mutant Strains. | ||
| International - Control Pricing Information for Genetically Engineered Mutant Strains. | ||
General Terms and Conditions
See Terms of Use
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