Strain Name:

NOR.Cg-Tg(Ins2-CD80)3B7Flv/LwnJ

Stock Number:

005714

Availability:

Repository-Cryopreserved

Use Restrictions Apply, see Terms of Use
Common Names: NOR.RIP-B7.1;     NOR.RIP-CD80;    

Description

Strain Information

Former Names NOR.Cg-Tg(Ins2-CD80)3B7Flv/FswJ    (Changed: 07-MAR-06 )
Type Congenic; Mutant Strain; Transgenic;
Additional information on Genetically Engineered Mutant Mice.
Specieslaboratory mouse
Background Strain NOR/Lt
Donor Strain (C57BL/6 X CBA)F2
H2 Haplotypeg7
GenerationN11p+F2N1
 
Donating Investigator Li Wen,   Yale School of Medicine

Appearance
albino, pink eyed
Related Genotype: A/A Tyrc/Tyrc

Description
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 50% of the NOR (backcross 5) transgenic mice become diabetic by 30 weeks of age compared the control NOR which is diabetes resistant. Spleens of diabetic NOR transgenic mice used in adoptive transfer experiments transfer diabetes to NOD.scid/RIP-B7.1 and irradiated non-diabetic NOR.Cg-Tg(Ins2-CD80)3B7Flv/FswJ mice, yet failed to transfer disease to NOD.scid, B6.scid, or CB17.scid.

NOR.-Tg(Ins2-CD80)3B7Flv/FswJ provides a tool for studying mechanisms for 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 and subsequently mated to NOR/Lt or BALB/c for 10 generations and B6.Cg-H2g7 for 1 generation. In 2005, The Jackson Laboratory received this NOR.Cg-Tg(Ins2-CD80)3B7Flv/FswJ at N10.

Control Information

  Control
   002050 NOR/LtJ (approximate)
 
  Considerations for Choosing Controls

Related Strains

Strains carrying   Tg(Ins2-CD80)3B7Flv allele
005715   B6.Cg H2g7-Tg(Ins2-CD80)3B7Flv/LwnJ
005713   C.Cg-Tg(Ins2-CD80)3B7Flv/LwnJ
004346   NOD.Cg-Prkdcscid Tg(Ins2-CD80)3B7Flv/DvsJ
View Strains carrying   Tg(Ins2-CD80)3B7Flv     (3 strains)

Strains carrying other alleles of Ins2
005534   B10.Cg-H2d Tg(Ins2-HA)165Bri/ShrmJ
005500   B6.C-Tg(Ins2-GP)34-20Olds/MvhJ
004826   B6.Cg-Tg(Ins2-NP)25-3Olds/MhvJ
003573   B6.Cg-Tg(Ins2-cre)25Mgn/J
005533   C.Cg-Tg(Ins2-HA)165Bri/ShrmJ
004827   C.Cg-Tg(Ins2-NP)25-3Olds/MvhJ
005432   C57BL/6-Tg(Ins2-OVA)307Wehi/WehiJ
005433   C57BL/6-Tg(Ins2-OVA)59Wehi/WehiJ
005431   C57BL/6-Tg(Ins2-TFRC/OVA)296Wehi/WehiJ
005564   FVB(Cg)-Tg(Ins2-CALM1)26Ove Tg(Cryaa-TAg)1Ove/PneJ
008232   FVB/N-Tg(Ins2-IAPP)RHFSoel/J
005522   NOD-Tg(Ins2*Y16A)1Ell/GseJ
005523   NOD-Tg(Ins2*Y16A)3Ell/GseJ
003499   NOD-Tg(Ins2-Fasl)24Ach
007840   NOD.Cg-Prkdcscid Tg(Ins2-CD86)12B70Flv/FswJ
004230   NOD.Cg-Prkdcscid Tg(Ins2-E3)1Dvs/DvsJ
003843   NOD.Cg-Prkdcscid Tg(Ins2-GAD2)1Lt/LtJ
003844   NOD.Cg-Prkdcscid Tg(Ins2-GAD2)2Lt/LtJ
005524   NOD.Cg-Tg(Ins2*Y16A)1Ell Ins1tm1Jja Ins2tm1Jja/GseJ
005525   NOD.Cg-Tg(Ins2*Y16A)3Ell Ins1tm1Jja Ins2tm1Jja/GseJ
006254   NOD.Cg-Tg(Ins2-Ccl21b)2Cys/JbsJ
006154   NOD.Cg-Tg(Ins2-Cxcl13)1Cys/JbsJ
003869   NOD.Cg-Tg(Ins2-E3)1Dvs/DvsJ
005685   NOD.Cg-Tg(Ins2-HA)165Bri/ShrmJ
002380   NOD.Cg-Tg(Ins2-TAg)1Lt Prkdcscid/DvsJ
004602   NOD.Cg-Tg(Ins2-rtTA)2Doi/DoiJ
004937   NOD.Cg-Tg(Ins2-tTA)1Doi/DoiJ
005734   NOD/Lt-Tg(Ins2-rtTA)1Ach/AchJ
005870   NOD/ShiLt(Cg)-Tg(Ins2-GAD2)2Lt/J
006777   NOD/ShiLt-Tg(Ins2-Cd274)2Mdos/MdosJ
005733   NOD/ShiLt-Tg(Ins2-Fas*I246N)1Ach/AchJ
003074   NOD/ShiLt-Tg(Ins2-GAD2)1Lt/LtJ
004986   NOD/ShiLt-Tg(Ins2-cre)3Lt/Lt
003855   NOD/ShiLt-Tg(Ins2-cre)5Lt/LtJ
004987   NOD/ShiLt-Tg(Ins2-cre)6Lt/Lt
002033   NOD/ShiLt-Tg(RipTAg)1Lt/J
004226   NOD/ShiLtDvs-Tg(Ins2-E3*309)5Dvs/DvsJ
004227   NOD/ShiLtDvs-Tg(Ins2-E3*704)2Dvs/DvsJ
004968   NOD/ShiLtDvs-Tg(Ins2-E3*734)3Dvs/DvsJ
004990   NOD/ShiLtDvs-Tg(Ins2-E3*734)4Dvs/DvsJ
008122   STOCK Tg(Ins2-cre/Esr1)1Dam/J
008250   STOCK Tg(Ins2-rtTA)2Efr/J
View Strains carrying other alleles of Ins2     (42 strains)

Additional Web Information

Congenic Nomenclature

Phenotype

Phenotype Information

View Related Disease (OMIM) Terms

View Mammalian Phenotype Terms

Mammalian Phenotype Terms
      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
View Research Applications

Research Applications
This mouse can be used to support research in many areas including:

Diabetes 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

Genes & Alleles

Gene & Allele Information

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, STD PCR, vers. 1

Helpful Links

Optimizing PCR Protocols

References

References

Additional References

Tg(Ins2-CD80)3B7Flv related

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 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]

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 View International pricing
Weeks of AgePrice*Gender
Cryorecovery Fee $1900.00
*Price(s) in US dollars ($)

Additional Supply Details

Pricing for International shipping destinations View USA Canada and Mexico pricing
Weeks of AgePrice*Gender
Cryorecovery Fee $2470.00
*Price(s) in US dollars ($)

Additional Supply Details

Supply Details

Standard SupplyRepository-Cryopreserved. Must Be Recovered. Please refer to pricing and supply notes for further information.
Supply Notes
  • Cryorecovery - Standard.
    The recovery process begins when a signed agreement form is returned to the Customer Service Department after order placement. Although results vary by strain, at least two males and two females (two pairs) will be provided, typically within 15 weeks of our receipt of the signed agreement form. If the first recovery attempt is unsuccessful or only one pair is recovered, a second recovery will be done, extending the delivery time to approximately 25 weeks. At least one member of each pair will be of known genotype and will carry the mutation if it is a mutant strain. Please note that pairs may not reflect the mating scheme utilized by The Jackson Laboratory prior to cryopreservation of the strain. Mating schemes are sometimes modified for successful cryopreservation. Price represents a repository maintenance fee, which includes the cost of recovery of the strain from the cryopreservation resource and the periodic replacement of the frozen embryos used for recovery.

    Cryorecovery to establish a Dedicated Supply for greater quantities of mice.
    One to two pairs will be recovered to establish a Dedicated Supply of mice. Price by quotation. For more information on Dedicated Supply, please contact JAX® Services, Tel: 1-800-422-6423 or 1-207-288-5845.

  • This strain is included in the Type 1 Diabetes Repository collection.

Control Information

  Control
   002050 NOR/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.

General Terms and Conditions


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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.
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fax:207-288-6655

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