Strain Name:

B6.Cg H2g7-Tg(Ins2-CD80)3B7Flv/LwnJ

Stock Number:

005715

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Availability:

Cryopreserved - Ready for recovery

Use Restrictions Apply, see Terms of Use
Common Names: B6.H2g7-RIP-B7.1;     B6.H2g7-RIP-CD80;     B6.H2g7-RIPB7;    

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.
Specieslaboratory mouse
Background Strain B6.NOD-H2g7
Donor Strain (C57BL/6 X CBA)F2
H2 Haplotypeg7
GenerationN?F9+F2pN1
Generation Definitions
 
Donating Investigator Li Wen,   Yale School of Medicine

Appearance
black
Related Genotype: a/a

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. 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

View Strains carrying   H2g7     (15 strains)

Strains carrying   Tg(Ins2-CD80)3B7Flv allele
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
View Strains carrying   Tg(Ins2-CD80)3B7Flv     (3 strains)

Strains carrying other alleles of CD80
006778   NOD/ShiLt-Tg(GFAP-Cd80)9Mdos/MdosJ
View Strains carrying other alleles of CD80     (1 strain)

Strains carrying other alleles of H2
006500   129.NOD-(D17Mit175-H2)/J
001649   A.BY H2bc H2-T18f/SnJ-Dstncorn1/J
000140   A.BY-H2bc H2-T18f/SnJ
000472   A.CA-H2f H2-T18a/SnJ
000471   A.SW-H2s H2-T18b/SnJ
001066   A.TH-H2t2/SfDvEgMobJ
001067   A.TL-H2t1/SfDvEgMobJ
002089   AK.B6-H2b Fv1b/J
002090   AK.B6-H2b/J
001094   AK.L-H2b/1CyTyJ
001095   AK.L-H2oz2/CyJ
001096   AK.L-H2oz3/CyJ
000470   AK.M-H2m H2-T18a/nSnJ
000469   B10.A-H2a H2-T18a/SgSnJ
000468   B10.A-H2h2/(2R)SgSnJ
001150   B10.A-H2h4/(4R)SgDvEgJ
001149   B10.A-H2i3/(3R)SgDvEgJ
000467   B10.A-H2i5 H2-T18a/(5R)SgSnJ
000466   B10.AKM-H2m H2-T18a/SnJ
001954   B10.AQR-H2y1/KljMcdJ
000465   B10.BR-H2k2 H2-T18a/SgSnJ
004804   B10.BR-H2k2 H2-T18a/SgSnJJrep
005308   B10.Cg-H2d Tg(TcraCl4,TcrbCl4)1Shrm/ShrmJ
005534   B10.Cg-H2d Tg(Ins2-HA)165Bri/ShrmJ
010514   B10.Cg-H2g Tg(Cd4-Klra1)6295Dl/J
006446   B10.Cg-H2h4 Sh3pxd2bnee/GrsrJ
006102   B10.Cg-H2k Tg(Il2/NFAT-luc)83Rinc/J
006100   B10.Cg-H2k Tg(NFkB/Fos-luc)26Rinc/J
005895   B10.Cg-Thy1a H2d Tg(TcraCl1,TcrbCl1)1Shrm/J
002024   B10.D1-H2q/SgJ
001163   B10.D2-H2bm23/EgJ
000462   B10.D2-H2d/n2SnJ
001164   B10.D2-H2dm1/EgJ
001151   B10.D2-H2g3/(103R)EgJ
001153   B10.D2-H2i7/(107R)EgJ
001152   B10.D2-H2ia/(106R)EgJ
000460   B10.D2-Hc0 H2d H2-T18c/o2SnJ
000461   B10.D2-Hc0 H2d H2-T18c/oSnJ
000463   B10.D2-Hc1 H2d H2-T18c/nSnJ
003147   B10.D2-Hc1 H2d H2-T18c/nSnJ-Tg(DO11.10)10Dlo/J
000464   B10.DA-H2qp1 H2-T18b/(80NS)SnJ
001823   B10.F-H2bp5/(14R)J
001818   B10.F-H2pb1/(13R)J
001012   B10.HTG-H2g/2CyJ
000999   B10.HTG-H2g/3CyJ
001894   B10.LG-H2ar1/J
000459   B10.M-H2f H2-T18a?/SnJ
002225   B10.M-H2f/nMob Fmn1ld-2J/J
001068   B10.M-H2f/nMobJ
000739   B10.M-H2fm2/MobJ
001154   B10.MBR-H2bq1/SxEgJ
001825   B10.P-H2kp1/(10R)SgJ
003199   B10.PL-H2u H2-T18a/(73NS)Sn-Tg(TCRA)B1Jg/J
003200   B10.PL-H2u H2-T18a/(73NS)Sn-Tg(TCRB)C14Jg/J
000458   B10.PL-H2u H2-T18a/(73NS)SnJ
000457   B10.RIII-H2r H2-T18b/(71NS)SnJ
001069   B10.RIII-H2r/(71NS)nMobJ
001760   B10.S-H2as1/(8R)/J
001953   B10.S-H2s/SgMcdJ
001817   B10.S-H2sm1/(12R)SgJ
001650   B10.S-H2t4/(9R)/J
000456   B10.SM H2v H2-T18b/(70NS)Sn-cw/J
001155   B10.T-H2y2/(6R)SgDvEgJ
000445   B10.WB-H2j H2-T18b/SnJ
000444   B10.Y-H2pa H2-T18c/SnJ
003483   B6 x B10.D1-H2q/SgJ-Nox3het-2J/J
003561   B6 x B10.PL-H2u/(73NS)Sn-Hxl/J
002995   B6 x C.B10-H2b/LiMcdJ-Fbn2fp-2J/J
003584   B6.129S2-H2dlAb1-Ea/J
001148   B6.AK-H2k/FlaEgJ
001895   B6.AK-H2k/J
001160   B6.C-H2bm10/KhEgJ
001161   B6.C-H2bm11/KhEgJ
000364   B6.C-H2bm2/ByJ
000369   B6.C-H2bm4/ByJ
001158   B6.C-H2bm7/KhEgJ
000360   B6.C-H2d Mdmg1BALB/cBy/aByJ
000359   B6.C-H2d/bByJ
001429   B6.C-H2g6/J
007958   B6.Cg-H2b3/FlaCmwJ
007959   B6.Cg-H2b4/FlaCmwJ
000944   B6.SJL-H2b C3c/2CyJ
000966   B6.SJL-H2s C3c/1CyJ
000945   B6.SW/1CyJ
003374   B6;129S2-H2dlAb1-Ea/J
003240   B6;B10.A-H2a-Tg(H2KmPCC)2939Stoe/J
002844   BALB.5R-H2i5/LilJ
001165   BALB/c-H2dm2/KhEgJ
001041   BKS.B6-H2b/J
001892   BRVR.B10-H2b/J
001893   BRVR.D2-H2d/J
002845   C.B-H2b Tg(H2-Dd)D8Gja/LilJ
001952   C.B10-H2b/LilMcdJ
001768   C3.Cg-Irs1Sml H2b/GrsrJ
000443   C3.HTG-H2g H2-T18b?/SnJ
000441   C3.JK-H2j H2-T18b/SnJ
000440   C3.LG-H2ar1/CkcCyJ
000439   C3.NB-H2p H2-T18c?/SnJ
000438   C3.SW-H2b/SnJ
000473   C3H-H2o2 C4bb/SfSnJ
001156   C57BL/6J-H2bm3/EgJ
001157   C57BL/6Kh-H2bm5/KhEgJ
000437   D1.C-H2d H2-T18c/SnJ
000436   D1.DA-H2qp1/SnJ
000435   D1.LP-H2b H2-T18b?/SnJ
000434   LP.RIII-H2r H2-T18b/SnJ
001382   LT.MA-Glo1b H2d/J
001383   LT.MA-Glo1b H2k/J
002591   NOD.B10Sn-H2b/J
026243   NOD.Cg-(rs4135590-rs13480186) H2k2Tg(ILK3mHEL)3Ccg Tg(TcrHEL3A9)1Mmd/SlsgJ
026624   NOD.Cg-(rs6385855-rs13480186) H2k2Tg(ILK3mHEL)3Ccg Tg(TcrHEL3A9)1Mmd/SlsgJ
006935   NOD.Cg-H2b thnh/J
004447   NOD.Cg-H2h4/DilTacUmmJ
001626   NOD.NON-H2nb1/LtJ
002032   NOD.SW-H2q/J
001308   STOCK H2473a/J
003154   WLC.C-H2d/MorJ
003153   WLC.Cg-H2d Mtv2a/MorJ
View Strains carrying other alleles of H2     (118 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
018960   B6N.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
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
007840   NOD.Cg-Prkdcscid Tg(Ins2-CD86)12B70Flv/FswJ
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
023972   NOD.Cg-Tg(Ins2-cre/ERT)1Dam/SbwJ
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
002033   NOD/ShiLt-Tg(Ins2-TAg)1Lt/J
004986   NOD/ShiLt-Tg(Ins2-cre)3Lt/LtJ
003855   NOD/ShiLt-Tg(Ins2-cre)5Lt/LtJ
004987   NOD/ShiLt-Tg(Ins2-cre)6Lt/LtJ
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/ERT)1Dam/J
008755   STOCK Tg(Ins2-rtTA)2Efr Tg(teto-DTA)1Gfi/J
008250   STOCK Tg(Ins2-rtTA)2Efr/J
View Strains carrying other alleles of Ins2     (45 strains)

Phenotype

Phenotype Information

View Related Disease (OMIM) Terms

Related Disease (OMIM) Terms provided by MGI
- Characteristics of this human disease are associated with transgenes and other mutation types in the mouse.
Diabetes Mellitus, Insulin-Dependent; IDDM
View Mammalian Phenotype Terms

Mammalian Phenotype Terms provided by MGI
      assigned by genotype

The following phenotype information is associated with a similar, but not exact match to this JAX® Mice strain.

Tg(Ins2-CD80)3B7Flv/?

        involves: C57BL/6 * CBA/Ca * NOD/Caj
  • endocrine/exocrine gland phenotype
  • insulitis
    • H2g7 homozygous transgenic mice show islet disruption with lymphocytic (T and B cell) infiltration, similar to diabetic NOD controls   (MGI Ref ID J:26618)
    • 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   (MGI Ref ID J:26618)
  • immune system phenotype
  • increased susceptibility to autoimmune diabetes
    • 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   (MGI Ref ID J:26618)
    • 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   (MGI Ref ID J:26618)
  • insulitis
    • H2g7 homozygous transgenic mice show islet disruption with lymphocytic (T and B cell) infiltration, similar to diabetic NOD controls   (MGI Ref ID J:26618)
    • 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   (MGI Ref ID J:26618)
  • renal/urinary system phenotype
  • increased urine glucose level   (MGI Ref ID J:26618)
  • homeostasis/metabolism phenotype
  • increased circulating glucose level
    • transgenic mice exhibit blood glucose in excess of 13.9 mmol (250 mg/dl)   (MGI Ref ID J:26618)
  • increased urine glucose level   (MGI Ref ID J:26618)
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, Inflammation and Autoimmunity Research
CD Antigens, Antigen Receptors, and Histocompatibility Markers

Research Tools
Diabetes and Obesity Research

H2g7 related

Immunology, Inflammation and Autoimmunity Research
CD Antigens, Antigen Receptors, and Histocompatibility Markers

Genes & Alleles

Gene & Allele Information provided by MGI

 
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 (Inserted expressed sequence)
Common Name(s) RIP-B7; RIP-B7-1; RIP-B7.1; RIP-CD80;
Mutation Made ByDr. 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 provided by MGI

Additional References

H2g7 related

Auger JL; Haasken S; Steinert EM; Binstadt BA. 2012. Incomplete TCR-beta allelic exclusion accelerates spontaneous autoimmune arthritis in K/BxN TCR transgenic mice. Eur J Immunol 42(9):2354-62. [PubMed: 22706882]  [MGI Ref ID J:187944]

Bassi EJ; Moraes-Vieira PM; Moreira-Sa CS; Almeida DC; Vieira LM; Cunha CS; Hiyane MI; Basso AS; Pacheco-Silva A; Camara NO. 2012. Immune regulatory properties of allogeneic adipose-derived mesenchymal stem cells in the treatment of experimental autoimmune diabetes. Diabetes 61(10):2534-45. [PubMed: 22688334]  [MGI Ref ID J:208536]

Belizaire 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]

Choisy-Rossi CM; Holl TM; Pierce MA; Chapman HD; Serreze DV. 2004. Enhanced pathogenicity of diabetogenic T cells escaping a non-MHC gene-controlled near death experience. J Immunol 173(6):3791-800. [PubMed: 15356126]  [MGI Ref ID J:167508]

Driver JP; Chen YG; Zhang W; Asrat S; Serreze DV. 2011. Unmasking genes in a type 1 diabetes-resistant mouse strain that enhances pathogenic CD8 T-cell responses. Diabetes 60(4):1354-9. [PubMed: 21307079]  [MGI Ref ID J:171763]

Driver JP; Scheuplein F; Chen YG; Grier AE; Wilson SB; Serreze DV. 2010. Invariant natural killer T-cell control of type 1 diabetes: a dendritic cell genetic decision of a silver bullet or Russian roulette. Diabetes 59(2):423-32. [PubMed: 19903740]  [MGI Ref ID J:164162]

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]

Fousteri G; Jasinski J; Dave A; Nakayama M; Pagni P; Lambolez F; Juntti T; Sarikonda G; Cheng Y; Croft M; Cheroutre H; Eisenbarth G; von Herrath M. 2012. Following the fate of one insulin-reactive CD4 T cell: conversion into Teffs and Tregs in the periphery controls diabetes in NOD mice. Diabetes 61(5):1169-79. [PubMed: 22403296]  [MGI Ref ID J:196727]

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]

Haasken S; Auger JL; Taylor JJ; Hobday PM; Goudy BD; Titcombe PJ; Mueller DL; Binstadt BA. 2013. Macrophage scavenger receptor 1 (Msr1, SR-A) influences B cell autoimmunity by regulating soluble autoantigen concentration. J Immunol 191(3):1055-62. [PubMed: 23794629]  [MGI Ref ID J:205440]

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 JS; Scandiuzzi L; Ray A; Wei J; Hofmeyer KA; Abadi YM; Loke P; Lin J; Yuan J; Serreze DV; Allison JP; Zang X. 2012. B7x in the periphery abrogates pancreas-specific damage mediated by self-reactive CD8 T cells. J Immunol 189(8):4165-74. [PubMed: 22972920]  [MGI Ref ID J:190522]

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]

Ma YD; Park C; Zhao H; Oduro KA Jr; Tu X; Long F; Allen PM; Teitelbaum SL; Choi K. 2009. Defects in osteoblast function but no changes in long-term repopulating potential of hematopoietic stem cells in a mouse chronic inflammatory arthritis model. Blood 114(20):4402-10. [PubMed: 19759358]  [MGI Ref ID J:154922]

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]

Martinez RJ; Zhang N; Thomas SR; Nandiwada SL; Jenkins MK; Binstadt BA; Mueller DL. 2012. Arthritogenic self-reactive CD4+ T cells acquire an FR4hiCD73hi anergic state in the presence of Foxp3+ regulatory T cells. J Immunol 188(1):170-81. [PubMed: 22124124]  [MGI Ref ID J:180819]

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]

Perera J; Meng L; Meng F; Huang H. 2013. Autoreactive thymic B cells are efficient antigen-presenting cells of cognate self-antigens for T cell negative selection. Proc Natl Acad Sci U S A 110(42):17011-6. [PubMed: 24082098]  [MGI Ref ID J:202000]

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]

Suwanai H; Wilcox MA; Mathis D; Benoist C. 2010. A defective Il15 allele underlies the deficiency in natural killer cell activity in nonobese diabetic mice. Proc Natl Acad Sci U S A 107(20):9305-10. [PubMed: 20439722]  [MGI Ref ID J:160284]

Taylor JJ; Martinez RJ; Titcombe PJ; Barsness LO; Thomas SR; Zhang N; Katzman SD; Jenkins MK; Mueller DL. 2012. Deletion and anergy of polyclonal B cells specific for ubiquitous membrane-bound self-antigen. J Exp Med 209(11):2065-77. [PubMed: 23071255]  [MGI Ref ID J:190897]

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]

Wang JX; Bair AM; King SL; Shnayder R; Huang YF; Shieh CC; Soberman RJ; Fuhlbrigge RC; Nigrovic PA. 2012. Ly6G ligation blocks recruitment of neutrophils via a beta2-integrin-dependent mechanism. Blood 120(7):1489-98. [PubMed: 22661700]  [MGI Ref ID J:189105]

Wei J; Loke P; Zang X; Allison JP. 2011. Tissue-specific expression of B7x protects from CD4 T cell-mediated autoimmunity. J Exp Med 208(8):1683-94. [PubMed: 21727190]  [MGI Ref ID J:177612]

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]

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]

Tg(Ins2-CD80)3B7Flv related

Alkanani AK; Hara N; Lien E; Ir D; Kotter CV; Robertson CE; Wagner BD; Frank DN; Zipris D. 2014. Induction of diabetes in the RIP-B7.1 mouse model is critically dependent on TLR3 and MyD88 pathways and is associated with alterations in the intestinal microbiome. Diabetes 63(2):619-31. [PubMed: 24353176]  [MGI Ref ID J:209068]

Brosi H; Reiser M; Rajasalu T; Spyrantis A; Oswald F; Boehm BO; Schirmbeck R. 2009. Processing in the endoplasmic reticulum generates an epitope on the insulin A chain that stimulates diabetogenic CD8 T cell responses. J Immunol 183(11):7187-95. [PubMed: 19890053]  [MGI Ref ID J:157398]

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; Meyerhoff J; Flavell R. 1994. The role of the T cell costimulator B7-1 in autoimmunity and the induction and maintenance of tolerance to peripheral antigen. Immunity 1(2):155-66. [PubMed: 7534199]  [MGI Ref ID J:189429]

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]

Rajasalu T; Brosi H; Schuster C; Spyrantis A; Boehm BO; Chen L; Reimann J; Schirmbeck R. 2010. Deficiency in B7-H1 (PD-L1)/PD-1 coinhibition triggers pancreatic beta-cell destruction by insulin-specific, murine CD8 T-cells. Diabetes 59(8):1966-73. [PubMed: 20484136]  [MGI Ref ID J:169352]

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

Animal Health Reports

Production of mice from cryopreserved embryos or sperm occurs in a maximum barrier room, G200.

Pricing and Purchasing

Pricing, Supply Level & Notes, Controls


Pricing for USA, Canada and Mexico shipping destinations View International Pricing

Cryopreserved

Cryopreserved Mice - Ready for Recovery

Price (US dollars $)
Cryorecovery* $2140.00
Animals Provided

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.

Standard Supply

Cryopreserved. Ready for recovery. Please refer to pricing and supply notes on the strain data sheet for further information.

Supply Notes

  • Cryorecovery - Standard.
    Progeny testing is not required.

    The average number of mice provided from recovery of our cryopreserved strains is 10. The total number of animals provided, their gender and genotype will vary. We will fulfill your order by providing at least two pair of mice, at least one animal of each pair carrying the mutation of interest. Please inquire if larger numbers of animals with specific genotype and genders are needed. Animals typically ship between 10 and 14 weeks from the date of your order. If a second cryorecovery is needed in order to provide the minimum number of animals, animals will ship within 25 weeks. IMPORTANT NOTE: The genotypes of animals provided may not reflect the mating scheme utilized by The Jackson Laboratory prior to cryopreservation, or that discussed in the strain description. Please inquire about possible genotypes which will be recovered for this specific strain. The Jackson Laboratory cannot guarantee the reproductive success of mice shipped to your facility. If the mice are lost after the first three days (post-arrival) or do not produce progeny at your facility, a new order and fee will be necessary.

    Cryorecovery to establish a Dedicated Supply for greater quantities of mice. Mice recovered can be used to establish a dedicated colony to contractually supply you mice according to your requirements. Price by quotation. For more information on Dedicated Supply, please contact JAX® Services, Tel: 1-800-422-6423 (from U.S.A., Canada or Puerto Rico only) or 1-207-288-5845 (from any location).

Pricing for International shipping destinations View USA Canada and Mexico Pricing

Cryopreserved

Cryopreserved Mice - Ready for Recovery

Price (US dollars $)
Cryorecovery* $2782.00
Animals Provided

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.

Standard Supply

Cryopreserved. Ready for recovery. Please refer to pricing and supply notes on the strain data sheet for further information.

Supply Notes

  • Cryorecovery - Standard.
    Progeny testing is not required.

    The average number of mice provided from recovery of our cryopreserved strains is 10. The total number of animals provided, their gender and genotype will vary. We will fulfill your order by providing at least two pair of mice, at least one animal of each pair carrying the mutation of interest. Please inquire if larger numbers of animals with specific genotype and genders are needed. Animals typically ship between 10 and 14 weeks from the date of your order. If a second cryorecovery is needed in order to provide the minimum number of animals, animals will ship within 25 weeks. IMPORTANT NOTE: The genotypes of animals provided may not reflect the mating scheme utilized by The Jackson Laboratory prior to cryopreservation, or that discussed in the strain description. Please inquire about possible genotypes which will be recovered for this specific strain. The Jackson Laboratory cannot guarantee the reproductive success of mice shipped to your facility. If the mice are lost after the first three days (post-arrival) or do not produce progeny at your facility, a new order and fee will be necessary.

    Cryorecovery to establish a Dedicated Supply for greater quantities of mice. Mice recovered can be used to establish a dedicated colony to contractually supply you mice according to your requirements. Price by quotation. For more information on Dedicated Supply, please contact JAX® Services, Tel: 1-800-422-6423 (from U.S.A., Canada or Puerto Rico only) or 1-207-288-5845 (from any location).

View USA Canada and Mexico Pricing View International Pricing

Standard Supply

Cryopreserved. Ready for recovery. Please refer to pricing and supply notes on the strain data sheet for further information.

General Supply Notes

Control Information

  Control
   003300 B6.NOD-(D17Mit21-D17Mit10)/LtJ (approximate)
 
  Considerations for Choosing Controls
  Control Pricing Information for Genetically Engineered Mutant Strains.
 

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Terms are granted by individual review and stated on the customer invoice(s) and account statement. These transactions are payable in U.S. currency within the granted terms. Payment for services, products, shipping containers, and shipping costs that are rendered are expected within the payment terms indicated on the invoice or stated by contract. Invoices and account balances in arrears of stated terms may result in The Jackson Laboratory pursuing collection activities including but not limited to outside agencies and court filings.


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The Jackson Laboratory's Genotype Promise

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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- Use of MICE by companies or for-profit entities requires a license prior to shipping.

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phone:207-288-6470

JAX® Mice, Products & Services Conditions of Use

"MICE" means mouse strains, their progeny derived by inbreeding or crossbreeding, unmodified derivatives from mouse strains or their progeny supplied by The Jackson Laboratory ("JACKSON"). "PRODUCTS" means biological materials supplied by JACKSON, and their derivatives. "RECIPIENT" means each recipient of MICE, PRODUCTS, or services provided by JACKSON including each institution, its employees and other researchers under its control. MICE or PRODUCTS shall not be: (i) used for any purpose other than the internal research, (ii) sold or otherwise provided to any third party for any use, or (iii) provided to any agent or other third party to provide breeding or other services. Acceptance of MICE or PRODUCTS from JACKSON shall be deemed as agreement by RECIPIENT to these conditions, and departure from these conditions requires JACKSON's prior written authorization.

No Warranty

MICE, PRODUCTS AND SERVICES ARE PROVIDED “AS IS”. JACKSON EXTENDS NO WARRANTIES OF ANY KIND, EITHER EXPRESS, IMPLIED, OR STATUTORY, WITH RESPECT TO MICE, PRODUCTS OR SERVICES, INCLUDING ANY IMPLIED WARRANTY OF MERCHANTABILITY OR FITNESS FOR A PARTICULAR PURPOSE, OR ANY WARRANTY OF NON-INFRINGEMENT OF ANY PATENT, TRADEMARK, OR OTHER INTELLECTUAL PROPERTY RIGHTS.

In case of dissatisfaction for a valid reason and claimed in writing by a purchaser within ninety (90) days of receipt of mice, products or services, JACKSON will, at its option, provide credit or replacement for the mice or product received or the services provided.

No Liability

In no event shall JACKSON, its trustees, directors, officers, employees, and affiliates be liable for any causes of action or damages, including any direct, indirect, special, or consequential damages, arising out of the provision of MICE, PRODUCTS or services, including economic damage or injury to property and lost profits, and including any damage arising from acts or negligence on the part of JACKSON, its agents or employees. Unless prohibited by law, in purchasing or receiving MICE, PRODUCTS or services from JACKSON, purchaser or recipient, or any party claiming by or through them, expressly releases and discharges JACKSON from all such causes of action or damages, and further agrees to defend and indemnify JACKSON from any costs or damages arising out of any third party claims.

MICE and PRODUCTS are to be used in a safe manner and in accordance with all applicable governmental rules and regulations.

The foregoing represents the General Terms and Conditions applicable to JACKSON’s MICE, PRODUCTS or services. In addition, special terms and conditions of sale of certain MICE, PRODUCTS or services may be set forth separately in JACKSON web pages, catalogs, price lists, contracts, and/or other documents, and these special terms and conditions shall also govern the sale of these MICE, PRODUCTS and services by JACKSON, and by its licensees and distributors.

Acceptance of delivery of MICE, PRODUCTS or services shall be deemed agreement to these terms and conditions. No purchase order or other document transmitted by purchaser or recipient that may modify the terms and conditions hereof, shall be in any way binding on JACKSON, and instead the terms and conditions set forth herein, including any special terms and conditions set forth separately, shall govern the sale of MICE, PRODUCTS or services by JACKSON.


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