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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Tg(Ins2-CD80)3B7Flv
transgene insertion 3B7, Richard Flavell
MGI:2682826
Summary 9 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
cx1
H2-Ab1b-tm1Gru/H2-Ab1b-tm1Gru
Tg(HLA-DQA1,HLA-DQB1)1Dv/0
Tg(Ins2-CD80)3B7Flv/0
B6.Cg-H2-Ab1b-tm1Gru Tg(HLA-DQA1,HLA-DQB1)1Dv Tg(Ins2-CD80)3B7Flv MGI:3623405
cx2
Tg(HLA-DQA1,HLA-DQB1)1Dv/0
Tg(Ins2-CD80)3B7Flv/0
B6.Cg-Tg(HLA-DQA1,HLA-DQB1)1Dv Tg(Ins2-CD80)3B7Flv MGI:3623410
cx3
H2-Ab1b-tm1Gru/H2-Ab1b-tm1Gru
Tg(HLA-DQA1,HLA-DQB1)1Dv/0
Tg(Ins2-CD80)3B7Flv/0
involves: 129S2/SvPas * C57BL/6 * C57BL/10SnJ * CBA MGI:3639135
cx4
H2-Ab1b-tm1Gru/H2-Ab1b-tm1Gru
Tg(HLA-DQA1,HLA-DQB1)1Dv/0
Tg(HLA-DRB1)31Dmz/0
Tg(Ins2-CD80)3B7Flv/0
involves: 129S2/SvPas * C57BL/6 * C57BL/10SnJ * CBA * SJL MGI:3639133
cx5
H2-Ab1b-tm1Gru/H2-Ab1b-tm1Gru
Tg(Ins2-CD80)3B7Flv/0
involves: 129S2/SvPas * C57BL/6 * CBA MGI:3639140
cx6
H2-Ab1b-tm1Gru/H2-Ab1b-tm1Gru
Tg(HLA-DRB1)31Dmz/0
Tg(Ins2-CD80)3B7Flv/0
involves: 129S2/SvPas * C57BL/6 * CBA * SJL MGI:3639130
cx7
Tg(Ins2-CD80)3B7Flv/0
Tg(Ins2-Tnf)17Flv/0
involves: C57BL/6 * CBA/Ca MGI:3766038
cx8
Tg(Ins2-CD80)3B7Flv/0
Tg(Ins2-H2-Ead,Ins2-H2-Eb1b)187-7Bri/0
involves: C57BL/6 * CBA/Ca * SJL MGI:3766042
tg9
Tg(Ins2-CD80)3B7Flv/? involves: C57BL/6 * CBA/Ca * NOD/Caj MGI:3757580


Genotype
MGI:3623405
cx1
Allelic
Composition
H2-Ab1b-tm1Gru/H2-Ab1b-tm1Gru
Tg(HLA-DQA1,HLA-DQB1)1Dv/0
Tg(Ins2-CD80)3B7Flv/0
Genetic
Background
B6.Cg-H2-Ab1b-tm1Gru Tg(HLA-DQA1,HLA-DQB1)1Dv Tg(Ins2-CD80)3B7Flv
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
H2-Ab1b-tm1Gru mutation (11 available); any H2-Ab1 mutation (81 available)
Tg(HLA-DQA1,HLA-DQB1)1Dv mutation (3 available)
Tg(Ins2-CD80)3B7Flv mutation (5 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
immune system
• diabetic transgenic mice display sialadenitis
• over 80% of transgenic mice develop diabetes (positive urine glucose test and >250 mg/dl blood glucose) beginning at 4 months of age

homeostasis/metabolism
• over 80% have blood glucose levels above 250 mg/dl
• seen in over 80% of mice

digestive/alimentary system
• diabetic transgenic mice display sialadenitis

endocrine/exocrine glands
• diabetic transgenic mice display sialadenitis

renal/urinary system
• seen in over 80% of mice

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
type 1 diabetes mellitus DOID:9744 OMIM:222100
J:59245




Genotype
MGI:3623410
cx2
Allelic
Composition
Tg(HLA-DQA1,HLA-DQB1)1Dv/0
Tg(Ins2-CD80)3B7Flv/0
Genetic
Background
B6.Cg-Tg(HLA-DQA1,HLA-DQB1)1Dv Tg(Ins2-CD80)3B7Flv
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(HLA-DQA1,HLA-DQB1)1Dv mutation (3 available)
Tg(Ins2-CD80)3B7Flv mutation (5 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
immune system
• none of the mice develop spontaneous diabetes over the 10-month observation period




Genotype
MGI:3639135
cx3
Allelic
Composition
H2-Ab1b-tm1Gru/H2-Ab1b-tm1Gru
Tg(HLA-DQA1,HLA-DQB1)1Dv/0
Tg(Ins2-CD80)3B7Flv/0
Genetic
Background
involves: 129S2/SvPas * C57BL/6 * C57BL/10SnJ * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
H2-Ab1b-tm1Gru mutation (11 available); any H2-Ab1 mutation (81 available)
Tg(HLA-DQA1,HLA-DQB1)1Dv mutation (3 available)
Tg(Ins2-CD80)3B7Flv mutation (5 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
immune system
• stimulated CD4+ T cells secrete increased levels of Ifng compared to either DR4-transgenic or double transgenic MHC class II-deficient mice
• stimulated CD4+ T cells secrete low levels of Il-6 compared to either DR4-transgenic or double transgenic MHC class II-deficient mice
• 73% of mice expressing the transgene develop diabetes (blood glucose >250 mg/dl) compared to 0% of nontransgenic MHC class II-deficient mice

homeostasis/metabolism
• 73% display blood glucose levels above 250 mg/dl
• seen in 73% of mice

renal/urinary system
• seen in 73% of mice




Genotype
MGI:3639133
cx4
Allelic
Composition
H2-Ab1b-tm1Gru/H2-Ab1b-tm1Gru
Tg(HLA-DQA1,HLA-DQB1)1Dv/0
Tg(HLA-DRB1)31Dmz/0
Tg(Ins2-CD80)3B7Flv/0
Genetic
Background
involves: 129S2/SvPas * C57BL/6 * C57BL/10SnJ * CBA * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
H2-Ab1b-tm1Gru mutation (11 available); any H2-Ab1 mutation (81 available)
Tg(HLA-DQA1,HLA-DQB1)1Dv mutation (3 available)
Tg(HLA-DRB1)31Dmz mutation (1 available)
Tg(Ins2-CD80)3B7Flv mutation (5 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
immune system
• transgenic mice develop sialadenitis and severity is associated with diabetes development
• coexpression of DR4 and DQ8 transgenes increases CD4+ T cell numbers 2-fold compared to either DR4 or DQ8 single transgenic line
• there are fewer CD8+ T cells in pancreatic infiltrates than in MHC class II-deficient mice expressing only DQ8
• incidence of diabetes (blood glucose >250 mg/dl; 5/22, 23%) is lowered from incidence in MHC class II-deficient mice expressing the DQ8 transgene (73%) and similar to deficient mice transgenic for DR4

endocrine/exocrine glands
• transgenic mice develop sialadenitis and severity is associated with diabetes development

hematopoietic system
• coexpression of DR4 and DQ8 transgenes increases CD4+ T cell numbers 2-fold compared to either DR4 or DQ8 single transgenic line
• there are fewer CD8+ T cells in pancreatic infiltrates than in MHC class II-deficient mice expressing only DQ8

digestive/alimentary system
• transgenic mice develop sialadenitis and severity is associated with diabetes development

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
type 1 diabetes mellitus DOID:9744 OMIM:222100
J:68641




Genotype
MGI:3639140
cx5
Allelic
Composition
H2-Ab1b-tm1Gru/H2-Ab1b-tm1Gru
Tg(Ins2-CD80)3B7Flv/0
Genetic
Background
involves: 129S2/SvPas * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
H2-Ab1b-tm1Gru mutation (11 available); any H2-Ab1 mutation (81 available)
Tg(Ins2-CD80)3B7Flv mutation (5 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
immune system
• only one of the MHC class II-deficient mice developed diabetes (blood glucose >250 mg/dl)




Genotype
MGI:3639130
cx6
Allelic
Composition
H2-Ab1b-tm1Gru/H2-Ab1b-tm1Gru
Tg(HLA-DRB1)31Dmz/0
Tg(Ins2-CD80)3B7Flv/0
Genetic
Background
involves: 129S2/SvPas * C57BL/6 * CBA * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
H2-Ab1b-tm1Gru mutation (11 available); any H2-Ab1 mutation (81 available)
Tg(HLA-DRB1)31Dmz mutation (1 available)
Tg(Ins2-CD80)3B7Flv mutation (5 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
• transgenic mice develop sialadenitis and severity is associated with diabetes development

immune system
• transgenic mice develop sialadenitis and severity is associated with diabetes development
• expression of the DR4 transgene increases CD4+ T cell numbers compared to the H2-Ab1-deficient Tg(Ins2-CD80)3B7Flv mice
• there are fewer CD8+ T cells in pancreatic infiltrates than in MHC class II-deficient mice expressing only DQ8
• incidence of diabetes (5/20) is lower than in MHC class II-deficient mice expressing the DQ8 transgene where incidence is 3-fold higher (73%)

hematopoietic system
• expression of the DR4 transgene increases CD4+ T cell numbers compared to the H2-Ab1-deficient Tg(Ins2-CD80)3B7Flv mice
• there are fewer CD8+ T cells in pancreatic infiltrates than in MHC class II-deficient mice expressing only DQ8

digestive/alimentary system
• transgenic mice develop sialadenitis and severity is associated with diabetes development

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
type 1 diabetes mellitus DOID:9744 OMIM:222100
J:68641




Genotype
MGI:3766038
cx7
Allelic
Composition
Tg(Ins2-CD80)3B7Flv/0
Tg(Ins2-Tnf)17Flv/0
Genetic
Background
involves: C57BL/6 * CBA/Ca
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(Ins2-CD80)3B7Flv mutation (5 available)
Tg(Ins2-Tnf)17Flv mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
immune system

homeostasis/metabolism




Genotype
MGI:3766042
cx8
Allelic
Composition
Tg(Ins2-CD80)3B7Flv/0
Tg(Ins2-H2-Ead,Ins2-H2-Eb1b)187-7Bri/0
Genetic
Background
involves: C57BL/6 * CBA/Ca * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(Ins2-CD80)3B7Flv mutation (5 available)
Tg(Ins2-H2-Ead,Ins2-H2-Eb1b)187-7Bri mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• diabetes-like symptoms (dehydration, weight loss) lead to death of most animals by 6 months of age

growth/size/body

immune system
• mice develop insulitis starting at ~5 months of age
• mice develop clinical signs of diabetes

endocrine/exocrine glands
• islet architecture becomes disorganized and islet tissue is replace by a ductal hyperplasia
• mice develop insulitis starting at ~5 months of age

homeostasis/metabolism




Genotype
MGI:3757580
tg9
Allelic
Composition
Tg(Ins2-CD80)3B7Flv/?
Genetic
Background
involves: C57BL/6 * CBA/Ca * NOD/Caj
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(Ins2-CD80)3B7Flv mutation (5 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
• 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
• 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
• 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

renal/urinary system

homeostasis/metabolism
• transgenic mice exhibit blood glucose in excess of 13.9 mmol (250 mg/dl)

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
type 1 diabetes mellitus DOID:9744 OMIM:222100
J:26618





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last database update
04/23/2024
MGI 6.23
The Jackson Laboratory