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- Description
- Phenotype
- Genes & alleles
- Genotyping
- Health & husbandry
- References
- Purchasing information
- Terms of Use
Description
The genotypes of the animals provided may not reflect those discussed in the strain description or the mating scheme utilized by The Jackson Laboratory prior to cryopreservation. Please inquire for possible genotypes for this specific strain.
Strain Information
Former Names B6.Cg-H2g7-Tg(Ins2-CD80)3B7Flv/LwnJ (Changed: 28-SEP-06 ) B6.Cg H2g7-Tg(Ins2-CD80)3B7Flv/FswJ (Changed: 07-MAR-06 ) Type Congenic; Major Histocompatibility Congenic; Mutant Strain; Transgenic; Additional information on Genetically Engineered and Mutant Mice. Visit our online Nomenclature tutorial. Additional information on Congenic nomenclature. Species laboratory mouse Background Strain B6.NOD-H2g7 Donor Strain (C57BL/6 X CBA)F2 H2 Haplotype g7 Generation N?F9+F2pN1 Donating Investigator Li Wen, Yale School of Medicine Appearance
black
Related Genotype: a/aDescription
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.
Development
A transgenic construct containing the human CD80 gene driven by the rat insulin promoter 1 (RIP) was injected fertilized eggs of a mating between C57BL/6 and CBA/Ca strains in the laboratory of Dr. Richard Flavell (Yale University). Founder animals were obtained and bred to C57BL/6 mice for more than 10 generations and subsequently mated to NOR/Lt or BALB/c for 10 generations and B6.NOD-H2g7 for 1 generation. In 2005, The Jackson Laboratory received this B6.Cg H2g7-Tg(Ins2-CD80)3B7Flv/LwnJ at N1F9.
Control Information
| Control | ||
|---|---|---|
| 003300 B6.NOD-(D17Mit21-D17Mit10)/LtJ | (approximate) | |
| Considerations for Choosing Controls | ||
Related Strains
Strains carrying H2g7 allele
View Strains carrying H2g7 (10 strains)
005713 C.Cg-Tg(Ins2-CD80)3B7Flv/LwnJ 004346 NOD.Cg-Prkdcscid Tg(Ins2-CD80)3B7Flv/DvsJ 005714 NOR.Cg-Tg(Ins2-CD80)3B7Flv/LwnJ
Additional Web Information
Genetic Quality Control Annual Report
Phenotype
Phenotype Information
assigned by genotype
The following phenotype information may relate to a genetic background differing from this JAX® Mice strain.
Tg(Ins2-CD80)3B7Flv/?
involves: C57BL/6 * CBA/Ca * NOD/Caj
- endocrine/exocrine gland phenotype
- insulitis (MGI Ref ID J:26618)
- H2g7 homozygous transgenic mice show islet disruption with lymphocytic (T and B cell) infiltration, similar to diabetic NOD controls
- N2 mice after a subsequent backcross to NOD show islet disruption with lymphocytic infiltration as early as 4 weeks while non-transgenic H2g7 homozygous or heterozygous littermates show varying degrees of insulitis by ~6 weeks
- immune system phenotype
- increased susceptibility to autoimmune diabetes (MGI Ref ID J:26618)
- 2/17 transgenic mice from the first cross to NOD develop diabetes between 10 and 14 weeks, compared to no diabetes in (NOD x C57BL/6)F1 non-transgenic controls
- after a further backcross to NOD, diabetes onset is accelerated relative to transgenic mice from the initial cross to NOD with some developing diabetes at 4 weeks; by 12 weeks, 46.2% of transgenic mice homozygous for H2g7 develop diabetes compared to no non-transgenic H2g7 homozygous littermates, or NOD controls which only start to exhibit diabetes at 12 weeks
- insulitis (MGI Ref ID J:26618)
- H2g7 homozygous transgenic mice show islet disruption with lymphocytic (T and B cell) infiltration, similar to diabetic NOD controls
- N2 mice after a subsequent backcross to NOD show islet disruption with lymphocytic infiltration as early as 4 weeks while non-transgenic H2g7 homozygous or heterozygous littermates show varying degrees of insulitis by ~6 weeks
- renal/urinary system phenotype
- increased urine glucose level (MGI Ref ID J:26618)
- homeostasis/metabolism phenotype
- increased circulating glucose level (MGI Ref ID J:26618)
- transgenic mice exhibit blood glucose in excess of 13.9 mmol (250 mg/dl)
- increased urine glucose level (MGI Ref ID J:26618)
- digestive/alimentary phenotype
- insulitis (MGI Ref ID J:26618)
- H2g7 homozygous transgenic mice show islet disruption with lymphocytic (T and B cell) infiltration, similar to diabetic NOD controls
- N2 mice after a subsequent backcross to NOD show islet disruption with lymphocytic infiltration as early as 4 weeks while non-transgenic H2g7 homozygous or heterozygous littermates show varying degrees of insulitis by ~6 weeks
This mouse can be used to support research in many areas including:
H2g7 relatedDiabetes and Obesity Research
Type 1 Diabetes (IDDM) Analysis Strains
NOD Transgenics
Immunology and Inflammation Research
CD Antigens, Antigen Receptors, and Histocompatibility Markers
Research Tools
Diabetes and Obesity Research
Immunology and Inflammation Research
CD Antigens, Antigen Receptors, and Histocompatibility Markers
Genes & Alleles
Gene & Allele Information
| Allele Symbol | H2g7 | ||
|---|---|---|---|
| Allele Name | g7 variant | ||
| Allele Type | Not Applicable | ||
| Gene Symbol and Name | H2, histocompatibility-2, MHC | ||
| Chromosome | 17 | ||
| Gene Common Name(s) | H-2; MHC-II; | ||
| General Note | The g7 variant has been observed in the following strains: DBR7, NON.NOD-H2g7 | ||
| Allele Symbol | Tg(Ins2-CD80)3B7Flv | ||
| Allele Name | transgene insertion 3B7, Richard Flavell | ||
| Allele Type | Transgenic (random, expressed) | ||
| Common Name(s) | RIP-B7; RIP-B7-1; RIP-B7.1; RIP-CD80; | ||
| Mutation Made By | Richard Flavell, Yale University School of Medicine | ||
| Strain of Origin | (C57BL/6 x CBA/Ca)F2 | ||
| Expressed Gene | CD80, CD80 molecule, human | ||
| Promoter | Ins2, insulin 2, rat | ||
| General Note | Mice carrying this transgene that also are homozygous for Prkdcscid are characterized by pancreatic beta cells that express a rat insulin II promoter regulated transgene encoding the human CD80 T cell co-stimulatory molecule. | ||
| Molecular Note | The transgene contains a human CD80 antigen gene driven by the rat insulin II promoter (Ins2). [MGI Ref ID J:88250] | ||
Genotyping
Genotyping Information
Genotyping Protocols
Tg(Ins2-CD80)3B7Flv, Standard PCR
Helpful Links
Genotyping resources and troubleshooting
References
References
Selected Reference(s)
Wong FS; Du W; Thomas IJ; Wen L. 2005. The influence of the major histocompatibility complex on development of autoimmune diabetes in RIP-B7.1 mice. Diabetes 54(7):2032-40. [PubMed: 15983204] [MGI Ref ID J:109830]
Additional References
H2g7 relatedTg(Ins2-CD80)3B7Flv relatedBelizaire R; Unanue ER. 2009. Targeting proteins to distinct subcellular compartments reveals unique requirements for MHC class I and II presentation. Proc Natl Acad Sci U S A 106(41):17463-8. [PubMed: 19805168] [MGI Ref ID J:153672]
Binstadt BA; Hebert JL; Ortiz-Lopez A; Bronson R; Benoist C; Mathis D. 2009. The same systemic autoimmune disease provokes arthritis and endocarditis via distinct mechanisms. Proc Natl Acad Sci U S A 106(39):16758-63. [PubMed: 19805369] [MGI Ref ID J:153217]
Carrasco-Marin E; Shimizu J; Kanagawa O; Unanue ER. 1996. The class II MHC I-Ag7 molecules from non-obese diabetic mice are poor peptide binders. J Immunol 156(2):450-8. [PubMed: 8543793] [MGI Ref ID J:30538]
Ferreira C; Singh Y; Furmanski AL; Wong FS; Garden OA; Dyson J. 2009. Non-obese diabetic mice select a low-diversity repertoire of natural regulatory T cells. Proc Natl Acad Sci U S A 106(20):8320-5. [PubMed: 19359477] [MGI Ref ID J:148537]
Fossati G; Cooke A; Papafio RQ; Haskins K; Stockinger B. 1999. Triggering a second T cell receptor on diabetogenic T cells can prevent induction of diabetes. J Exp Med 190(4):577-83. [PubMed: 10449528] [MGI Ref ID J:108724]
Gray D; Abramson J; Benoist C; Mathis D. 2007. Proliferative arrest and rapid turnover of thymic epithelial cells expressing Aire. J Exp Med 204(11):2521-8. [PubMed: 17908938] [MGI Ref ID J:126040]
Jasinski JM; Yu L; Nakayama M; Li MM; Lipes MA; Eisenbarth GS; Liu E. 2006. Transgenic insulin (B:9-23) T-cell receptor mice develop autoimmune diabetes dependent upon RAG genotype, H-2g7 homozygosity, and insulin 2 gene knockout. Diabetes 55(7):1978-84. [PubMed: 16804066] [MGI Ref ID J:111874]
Klein J; Figueroa F; David CS. 1983. H-2 haplotypes, genes and antigens: second listing. II. The H-2 complex. Immunogenetics 17(6):553-96. [PubMed: 6407984] [MGI Ref ID J:7097]
Kouskoff V; Korganow AS; Duchatelle V; Degott C; Benoist C; Mathis D. 1996. Organ-specific disease provoked by systemic autoimmunity. Cell 87(5):811-22. [PubMed: 8945509] [MGI Ref ID J:36815]
Lee MS; Mueller R; Wicker LS; Peterson LB; Sarvetnick N. 1996. IL-10 is necessary and sufficient for autoimmune diabetes in conjunction with NOD MHC homozygosity. J Exp Med 183(6):2663-8. [PubMed: 8676087] [MGI Ref ID J:153576]
Leiter EH. 1998. NOD Mice and Related Strains: Origins, Husbandry and Biology Introduction. In: NOD Mice and Related Strains: Research Applications in Diabetes, AIDS, Cancer, and Other Diseases. RG Landes, Austin. [MGI Ref ID J:110093]
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]
Luhder F; Katz J; Benoist C; Mathis D. 1998. Major histocompatibility complex class II molecules can protect from diabetes by positively selecting T cells with additional specificities. J Exp Med 187(3):379-87. [PubMed: 9449718] [MGI Ref ID J:108722]
Mahler M; Bristol IJ; Leiter EH; Workman AE; Birkenmeier EH; Elson CO; Sundberg JP. 1998. Differential susceptibility of inbred mouse strains to dextran sulfate sodium-induced colitis. Am J Physiol 274(3 Pt 1):G544-51. [PubMed: 9530156] [MGI Ref ID J:46553]
Mangada J; Pearson T; Brehm MA; Wicker LS; Peterson LB; Shultz LD; Serreze DV; Rossini AA; Greiner DL. 2009. Idd loci synergize to prolong islet allograft survival induced by costimulation blockade in NOD mice. Diabetes 58(1):165-73. [PubMed: 18984741] [MGI Ref ID J:146982]
Martin-Orozco N; Chen Z; Poirot L; Hyatt E; Chen A; Kanagawa O; Sharpe A; Mathis D; Benoist C. 2003. Paradoxical dampening of anti-islet self-reactivity but promotion of diabetes by OX40 ligand. J Immunol 171(12):6954-60. [PubMed: 14662903] [MGI Ref ID J:86926]
Pearson T; Markees TG; Serreze DV; Pierce MA; Marron MP; Wicker LS; Peterson LB; Shultz LD; Mordes JP; Rossini AA; Greiner DL. 2003. Genetic disassociation of autoimmunity and resistance to costimulation blockade-induced transplantation tolerance in nonobese diabetic mice. J Immunol 171(1):185-95. [PubMed: 12816997] [MGI Ref ID J:109845]
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]
Serreze DV; Gallichan WS; Snider DP; Croitoru K; Rosenthal KL; Leiter EH; Christianson GJ; Dudley ME; Roopenian DC. 1996. MHC class I-mediated antigen presentation and induction of CD8+ cytotoxic T-cell responses in autoimmune diabetes-prone NOD mice. Diabetes 45(7):902-8. [PubMed: 8666141] [MGI Ref ID J:33688]
Turley SJ; Lee JW; Dutton-Swain N; Mathis D; Benoist C. 2005. Endocrine self and gut non-self intersect in the pancreatic lymph nodes. Proc Natl Acad Sci U S A 102(49):17729-33. [PubMed: 16317068] [MGI Ref ID J:104385]
Victoratos P; Kollias G. 2009. Induction of autoantibody-mediated spontaneous arthritis critically depends on follicular dendritic cells. Immunity 30(1):130-42. [PubMed: 19119026] [MGI Ref ID J:143728]
Yoshida T; Jiang F; Honjo T; Okazaki T. 2008. PD-1 deficiency reveals various tissue-specific autoimmunity by H-2b and dose-dependent requirement of H-2g7 for diabetes in NOD mice. Proc Natl Acad Sci U S A 105(9):3533-8. [PubMed: 18299579] [MGI Ref ID J:132764]
Zhang C; Todorov I; Lin CL; Atkinson M; Kandeel F; Forman S; Zeng D. 2007. Elimination of insulitis and augmentation of islet beta cell regeneration via induction of chimerism in overtly diabetic NOD mice. Proc Natl Acad Sci U S A 104(7):2337-42. [PubMed: 17267595] [MGI Ref ID J:119749]
Devendra D; Jasinski J; Melanitou E; Nakayama M; Li M; Hensley B; Paronen J; Moriyama H; Miao D; Eisenbarth GS; Liu E. 2005. Interferon-alpha as a mediator of polyinosinic:polycytidylic acid-induced type 1 diabetes. Diabetes 54(9):2549-56. [PubMed: 16123342] [MGI Ref ID J:129147]
Devendra D; Paronen J; Moriyama H; Miao D; Eisenbarth GS; Liu E. 2004. Differential immune response to B:9-23 insulin 1 and insulin 2 peptides in animal models of type 1 diabetes. J Autoimmun 23(1):17-26. [PubMed: 15236749] [MGI Ref ID J:91669]
Guerder S; Eynon EE; Flavell RA. 1998. Autoimmunity without diabetes in transgenic mice expressing beta cell-specific CD86, but not CD80: parameters that trigger progression to diabetes. J Immunol 161(5):2128-40. [PubMed: 9725204] [MGI Ref ID J:93555]
Guerder S; Picarella DE; Linsley PS; Flavell RA. 1994. Costimulator B7-1 confers antigen-presenting-cell function to parenchymal tissue and in conjunction with tumor necrosis factor alpha leads to autoimmunity in transgenic mice. Proc Natl Acad Sci U S A 91(11):5138-42. [PubMed: 7515187] [MGI Ref ID J:88250]
Havari E; Lennon-Dumenil AM; Klein L; Neely D; Taylor JA; McInerney MF; Wucherpfennig KW; Lipes MA. 2004. Expression of the B7.1 costimulatory molecule on pancreatic beta cells abrogates the requirement for CD4 T cells in the development of type 1 diabetes. J Immunol 173(2):787-96. [PubMed: 15240665] [MGI Ref ID J:91915]
Marron MP; Graser RT; Chapman HD; Serreze DV. 2002. Functional evidence for the mediation of diabetogenic T cell responses by HLA-A2.1 MHC class I molecules through transgenic expression in NOD mice. Proc Natl Acad Sci U S A 99(21):13753-8. [PubMed: 12361980] [MGI Ref ID J:109851]
Rajagopalan G; Kudva YC; Chen L; Wen L; David CS. 2003. Autoimmune diabetes in HLA-DR3/DQ8 transgenic mice expressing the co-stimulatory molecule B7-1 in the beta cells of islets of Langerhans. Int Immunol 15(9):1035-44. [PubMed: 12917255] [MGI Ref ID J:85223]
Serra P; Amrani A; Yamanouchi J; Han B; Thiessen S; Utsugi T; Verdaguer J; Santamaria P. 2003. CD40 ligation releases immature dendritic cells from the control of regulatory CD4+CD25+ T cells. Immunity 19(6):877-89. [PubMed: 14670304] [MGI Ref ID J:86995]
Skak K; Haase C; Michelsen BK. 2005. Preservation of beta-cell function during immune-mediated, B7-1-dependent alpha-cell destruction. Eur J Immunol 35(9):2583-90. [PubMed: 16078275] [MGI Ref ID J:113486]
Stephens LA; Kay TW. 1995. Pancreatic expression of B7 co-stimulatory molecules in the non-obese diabetic mouse. Int Immunol 7(12):1885-95. [PubMed: 8746558] [MGI Ref ID J:30235]
Thomas IJ; Petrich de Marquesini LG; Ravanan R; Smith RM; Guerder S; Flavell RA; Wraith DC; Wen L; Wong FS. 2007. CD86 has sustained costimulatory effects on CD8 T cells. J Immunol 179(9):5936-46. [PubMed: 17947667] [MGI Ref ID J:138692]
Ueno A; Cho S; Cheng L; Wang Z; Wang B; Yang Y. 2005. Diabetes resistance/susceptibility in T cells of nonobese diabetic mice conferred by MHC and MHC-linked genes. J Immunol 175(8):5240-7. [PubMed: 16210629] [MGI Ref ID J:119112]
Wen L; Chen NY; Tang J; Sherwin R; Wong FS. 2001. The regulatory role of DR4 in a spontaneous diabetes DQ8 transgenic model. J Clin Invest 107(7):871-80. [PubMed: 11285306] [MGI Ref ID J:68641]
Wen L; Peng J; Li Z; Wong FS. 2004. The effect of innate immunity on autoimmune diabetes and the expression of Toll-like receptors on pancreatic islets. J Immunol 172(5):3173-80. [PubMed: 14978124] [MGI Ref ID J:88224]
Wen L; Wong FS; Tang J; Chen NY; Altieri M; David C; Flavell R; Sherwin R. 2000. In vivo evidence for the contribution of human histocompatibility leukocyte antigen (HLA)-DQ molecules to the development of diabetes. J Exp Med 191(1):97-104. [PubMed: 10620608] [MGI Ref ID J:59245]
Wong S; Guerder S; Visintin I; Reich EP; Swenson KE; Flavell RA; Janeway CA Jr. 1995. Expression of the co-stimulator molecule B7-1 in pancreatic beta-cells accelerates diabetes in the NOD mouse. Diabetes 44(3):326-9. [PubMed: 7533734] [MGI Ref ID J:26618]
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 |
|
Animals Provided
Price (US dollars $) Cryorecovery Fee $1900.00 At least two mice that carry the mutation (if it is a mutant strain) will be provided. Their genotypes may not reflect those discussed in the strain description. Please inquire for possible genotypes and see additional details below.
Additional Supply Details
| Pricing for International shipping destinations |
|
Animals Provided
Price (US dollars $) Cryorecovery Fee $2470.00 At least two mice that carry the mutation (if it is a mutant strain) will be provided. Their genotypes may not reflect those discussed in the strain description. Please inquire for possible genotypes and see additional details below.
Additional Supply Details
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Supply Details
| Standard Supply | Cryopreserved. Ready for recovery. Please refer to pricing and supply notes for further information. |
|---|---|
| Supply Notes |
|
Control Information
| Control | ||
|---|---|---|
| 003300 B6.NOD-(D17Mit21-D17Mit10)/LtJ | (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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The Jackson Laboratory has rigorous genetic quality control and mutant gene genotyping programs to ensure the genetic background of JAX® Mice strains as well as the genotypes of strains with identified molecular mutations. JAX® Mice strains are only made available to researchers after meeting our standards. However, the phenotype of each strain may not be fully characterized and/or captured in the strain data sheets. Therefore, we cannot guarantee a strain's phenotype will meet all expectations. To ensure that JAX® Mice will meet the needs of individual research projects or when requesting a strain that is new to your research, we suggest ordering and performing tests on a small number of mice to determine suitability for your particular project.Ordering and Purchasing Information
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