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Type Coisogenic; Mutant Strain; Transgenic; Additional information on Genetically Engineered Mutant Mice. Species laboratory mouse H2 Haplotype g7 Donating Investigator Leonard Harrison, Walter and Eliza Hall Institute of Medic Appearance
pink-eyed, albino
Related Genotype: A/A Tyrc/TyrcDescription
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 specific immunotherapeutic strategies for preventing T1D and other autoimmune diseases.Development
The H2-Ea-Ins2 transgene encodes the protein coding region of mouse preproinsulin II (Ins2) amplified from genomic NOD DNA, controlled by an MHC class II, I-E alphak, promoter. The transgenic fragment was directly injected into NOD/LtWehi oocytes and has been maintained on an NOD/LtWehi background. In 2005, the T1DR received NOD-Tg(H2-Ea-Ins2)1Wehi/WehiJ transgenic mice and mated to NOD/LtJ prior to mating Tg x Tg.
| Control | ||
|---|---|---|
| 001976 NOD/ShiLtJ | (approximate) | |
| Considerations for Choosing Controls | ||
Strains carrying other alleles of H2-Ea
002035 NOD/ShiLt-Tg(H2-Ead)12Lt/J 002034 NOD/ShiLt-Tg(H2-Ead)5Lt/J 001658 STOCK Tg(H2-Ea)16Dim/J 001901 STOCK Tg(H2-Ea*deltaX)16Dim/J 001812 STOCK Tg(H2-Ea*deltaY)54Dim/J View Strains carrying other alleles of H2-Ea (5 strains)
Strains carrying other alleles of Ins2
006860 B6.129-Ins2Akita Bdkrb2tm1Jfh/SmiJ 006580 B6.Cg-Ins2Akita Ldlrtm1Her/J 004369 B6.Cg-Rag1tm1Mom Ins2Akita/J 003548 C57BL/6-Ins2Akita/J 007562 D2.B6-Ins2Akita/MatbJ 006867 FVB.B6-Ins2Akita/MlnJ 005036 NOD.129S2(B6)-Ins2tm1Jja/GseJ 005524 NOD.Cg-Tg(Ins2*Y16A)1Ell Ins1tm1Jja Ins2tm1Jja/GseJ 005525 NOD.Cg-Tg(Ins2*Y16A)3Ell Ins1tm1Jja Ins2tm1Jja/GseJ View Strains carrying other alleles of Ins2 (9 strains)
View Related Disease (OMIM) Terms
View Mammalian Phenotype Terms
Mammalian Phenotype Terms
assigned by genotype
Tg(H2-Ea-Ins2)1Wehi/0
NOD/LtJWehi-Tg(H2-Ea-Ins2)1Wehi
- endocrine/exocrine gland phenotype
- *normal* endocrine/exocrine gland phenotype (MGI Ref ID J:100232)
- unlike wild-type NOD mice, transgenic NOD/LtWehi mice do not develop spontaneous diabetes
- whereas wildtype NOD mice are susceptible to diabetes induction by cyclophosphamide, no transgenic NOD/LtWehi mice became diabetic (defined as blood glucose > 11 mmol/l) after a single cyclophosphamide injection; following a second injection only one of ten developed diabetes, and it was more slowly progressive than in wild-type controls
- pancreata of transgenic NOD/LtWehi mice are almost entirely free of insulitis: 90% of 244 islets from 100-day-old female mice and 98% of 259 islets from 147-day-old males had no cellular infiltration, and the rest exhibited only a minimal degree of insulitis
- salivary gland inflammation (MGI Ref ID J:100232)
- the transgene does not affect the characteristic susceptibility of NOD mice to sialitis, the degree of which does not differ significantly between transgenic NOD/LtWis mice and control littermates
- immune system phenotype
- *normal* immune system phenotype (MGI Ref ID J:100232)
- pancreata of transgenic NOD/LtWehi mice are almost entirely free of insulitis: 90% of islets from 100-day-old female mice and 98% of those from 147-day-old males have no cellular infiltration, and the rest exhibit only a minimal degree of insulitis
- abnormal T cell proliferation (MGI Ref ID J:100232)
- spleen- and draining lymph node-derived T cells from wild-type and transgenic NOD/LtWehi mice exhibit statistically similar in vitro proliferative responses to peptides derived from proinsulin and GAD2 (GAD65) following immunization with these self antigens
- salivary gland inflammation (MGI Ref ID J:100232)
- the transgene does not affect the characteristic susceptibility of NOD mice to sialitis, the degree of which does not differ significantly between transgenic NOD/LtWis mice and control littermates
- digestive/alimentary phenotype
- salivary gland inflammation (MGI Ref ID J:100232)
- the transgene does not affect the characteristic susceptibility of NOD mice to sialitis, the degree of which does not differ significantly between transgenic NOD/LtWis mice and control littermates
- hematopoietic system phenotype
- abnormal T cell proliferation (MGI Ref ID J:100232)
- spleen- and draining lymph node-derived T cells from wild-type and transgenic NOD/LtWehi mice exhibit statistically similar in vitro proliferative responses to peptides derived from proinsulin and GAD2 (GAD65) following immunization with these self antigens
Tg(H2-Ea-Ins2)1Wehi/Tg(H2-Ea-Ins2)1Wehi
NOD/LtJWehi-Tg(H2-Ea-Ins2)1Wehi
- immune system phenotype
- *normal* immune system phenotype (MGI Ref ID J:117352)
- G6pc2206-214-specific T cells have cytotoxic potential in vitro but are 'ignorant' of their antigen
- dendritic cell antigen presentation to dendritic cells from wild-type NOD mice; antigen presenting cell function is not affected
- abnormal CD8-positive T cell morphology (MGI Ref ID J:117352)
- T cells specific for IGRP206-214 (G6pc2206-214) are almost undetectable in absence of priming in peripheral blood or lymphoid tissues in NOD mice expressing the transgene, at any age assayed, while such cells are readily detected and peak at 15 weeks of age in wild-type NOD controls
- decreased T cell proliferation (MGI Ref ID J:117352)
- G6pc2206-214-specific CD8+ T cells transferred from Tg(TcraTcrbNY8.3)1Pesa NOD mice proliferate with much lower efficiency compared to cells transferred to wild-type NOD hosts
- no regulatory T cell generation is indicated by thymic expression of autoantigens
- decreased anti-insulin autoantibody level (MGI Ref ID J:117352)
- mice do not show an insulin autoantibody response, compared to wild-type NOD controls
- hematopoietic system phenotype
- *normal* hematopoietic system phenotype (MGI Ref ID J:117352)
- abnormal CD8-positive T cell morphology (MGI Ref ID J:117352)
- T cells specific for IGRP206-214 (G6pc2206-214) are almost undetectable in absence of priming in peripheral blood or lymphoid tissues in NOD mice expressing the transgene, at any age assayed, while such cells are readily detected and peak at 15 weeks of age in wild-type NOD controls
- decreased T cell proliferation (MGI Ref ID J:117352)
- G6pc2206-214-specific CD8+ T cells transferred from Tg(TcraTcrbNY8.3)1Pesa NOD mice proliferate with much lower efficiency compared to cells transferred to wild-type NOD hosts
- no regulatory T cell generation is indicated by thymic expression of autoantigens
View Research Applications
Research Applications
This mouse can be used to support research in many areas including:
Ins2 relatedDiabetes and Obesity Research
Type 1 Diabetes (IDDM) (resistant)
Type 1 Diabetes (IDDM) Analysis Strains (NOD Transgenics)
Immunology and Inflammation Research
Autoimmunity (Type 1 Diabetes)
CD Antigens, Antigen Receptors, and Histocompatibility Markers
Research Tools
Diabetes and Obesity Research
Diabetes and Obesity Research
Type 1 Diabetes (IDDM) Analysis Strains (NOD/ShiLtJ Non-MHC Congenics)
Immunology and Inflammation Research
Autoimmunity (Type 1 Diabetes)
| Allele Symbol | Tg(H2-Ea-Ins2)1Wehi | ||
|---|---|---|---|
| Allele Name | transgene insertion 1, William and Eliza Hall Institute | ||
| Allele Type | Transgenic (random, expressed) | ||
| Mutation Made By | Leonard Harrison, Walter and Eliza Hall Institute of Medic | ||
| Strain of Origin | NOD/ShiLt | ||
| Expressed Gene | Ins2, insulin II, mouse, laboratory | ||
| Promoter | H2-Ea, histocompatibility 2, class II antigen E alpha, mouse, laboratory | ||
| General Note | Two lines of mice were created with this trasgenic construct on the NOD background. No distinction was made between them. | ||
| Molecular Note |
The transgene comprises nucleotides -1,903 through -39 of the 5' flanking sequence of the MHC Class II gene H2-Ea (k allele), containing the promoter, followed by a 909 base pair mouse (NOD strain) genomic DNA fragment containing the sequence encoding prepronsulin II and the SV40 small t intron and polyadenylation signal. Transgene-derived mRNA is detectable in spleen and thymus of transgenic NOD/LtWehi mice, but not of control littermates, by reverse transcription followed by PCR (RT/PCR) using either primers for H2-Eak and proinsulin or two proinsulin primers. Immunoreactive proinsulin is detectable in medium from cultured transgenic splenocytes only after 8 days' culture and at levels 10-2 - 10-3 times those of cultured islets or islet cells; levels are increased by culture with interferon gamma and tumor necrosis factor alpha. [MGI Ref ID J:100232] | ||
Genotyping Protocols
Tg(H2-Ea-Ins2)1Wehi, STD PCR, vers. 1
Helpful Links
Optimizing PCR Protocols
French MB; Allison J; Cram DS; Thomas HE; Dempsey-Collier M; Silva A; Georgiou HM; Kay TW; Harrison LC; Lew AM. 1997. Transgenic expression of mouse proinsulin II prevents diabetes in nonobese diabetic mice. Diabetes 46(1):34-9. [PubMed: 8971078] [MGI Ref ID J:100232]
Tg(H2-Ea-Ins2)1Wehi relatedKrishnamurthy B; Dudek NL; McKenzie MD; Purcell AW; Brooks AG; Gellert S; Colman PG; Harrison LC; Lew AM; Thomas HE; Kay TW. 2006. Responses against islet antigens in NOD mice are prevented by tolerance to proinsulin but not IGRP. J Clin Invest 116(12):3258-65. [PubMed: 17143333] [MGI Ref ID J:117352]
Krishnamurthy B; Mariana L; Gellert SA; Colman PG; Harrison LC; Lew AM; Santamaria P; Thomas HE; Kay TW. 2008. Autoimmunity to Both Proinsulin and IGRP Is Required for Diabetes in Nonobese Diabetic 8.3 TCR Transgenic Mice. J Immunol 180(7):4458-4464. [PubMed: 18354167] [MGI Ref ID J:132969]
Currently there no information available for this strain. This may be due to the supply level of this strain.
| Pricing for USA, Canada and Mexico shipping destinations |
|
*Price(s) in US dollars ($)
Weeks of Age Price* Gender Cryorecovery Fee $1900.00 Cryopreserved Embryos Fee $1600.00
| Pricing for International shipping destinations |
|
*Price(s) in US dollars ($)
Weeks of Age Price* Gender Cryorecovery Fee $2470.00 Cryopreserved Embryos Fee $2080.00
| Standard Supply | Repository-Cryopreserved. Must Be Recovered. Please refer to pricing and supply notes for further information. |
|---|---|
| Supply Notes |
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| Control | ||
|---|---|---|
| 001976 NOD/ShiLtJ | (approximate) | |
| 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. | ||
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