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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Tg(HLA-DQA1,HLA-DQB1)73Myl
transgene insertion 73, Myra A Lipes
MGI:3687023
Summary 2 genotypes


Genotype
MGI:3687026
cx1
Allelic
Composition
H2-Ab1b-tm1Gru/H2-Ab1b-tm1Gru
Tg(HLA-DQA1,HLA-DQB1)73Myl/0
Genetic
Background
NOD.Cg-H2-Ab1b-tm1Gru Tg(HLA-DQA1,HLA-DQB1)73Myl
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)73Myl mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• >50% of transgenics (lines 73 and 275) die by 40 weeks of age; line 70 mice do not show significant premature death

homeostasis/metabolism
• massive mural thrombi adjacent to damaged tissue in atria are observed
• consistent with congestive heart failure
• consistent with congestive heart failure
• upon necropsy, diseased mice show varying degrees of pleural effusions

cardiovascular system
• myocyte degeneration and vacuolization are observed in atria, consistent with myocarditis
• associated with myocarditis with lymphocytic infiltrates
• diseased mice upon death are found to have enlarged hearts with ischemic coloration
• most healthy-appearing mice display marked cardiac enlargement at 40 weeks
• ventricular inflammatory lesions are composed of large numbers of CD4+ and CD8+ T cells with many F4/80 macrophages and few B cells
• enlarged livers show changes characteristic of centrilobular hepatic necrosis and hemorrhage
• many transgenic mice display symptoms of congestive heart failure; line 70 transgenics do not develop symptoms of congestive heart failure
• hearts show extensive mononuclear infiltrates in the atria; ventricles show focal infiltrates
• myocarditis development is transgene- and NOD-specific; the transgenics all exhibit myocarditis

endocrine/exocrine glands
• observed in transgenic and non-transgenic littermates with equal frequency
• transgenic mice show insulitis, but pancreatic beta cell damage is not sufficient to result in clinical diabetes

immune system
• hearts show extensive mononuclear infiltrates in the atria; ventricles show focal infiltrates
• myocarditis development is transgene- and NOD-specific; the transgenics all exhibit myocarditis
• observed in transgenic and non-transgenic littermates with equal frequency
• transgenic mice show insulitis, but pancreatic beta cell damage is not sufficient to result in clinical diabetes
• transgenic mice line 73 show the highest prevalence and titers of cardiac tissue autoantibodies (16/18 mice are positive), while only 5/24 mice of line 70 are positive with lower antibody titers

liver/biliary system
• enlarged livers show changes characteristic of centrilobular hepatic necrosis and hemorrhage
• livers show pathological changes characteristic of severe cardiac insufficiency and centrilobular hepatic necrosis and hemorrhage
• upon necropsy, diseased mice show enlargement and darkening of the liver

digestive/alimentary system
• observed in transgenic and non-transgenic littermates with equal frequency

behavior/neurological
• consistent with congestive heart failure

muscle
• myocyte degeneration and vacuolization are observed in atria, consistent with myocarditis
• associated with myocarditis with lymphocytic infiltrates

respiratory system
• upon necropsy, diseased mice show varying degrees of pleural effusions
• mice show acute onset of labored breathing

growth/size/body
• diseased mice upon death are found to have enlarged hearts with ischemic coloration
• most healthy-appearing mice display marked cardiac enlargement at 40 weeks
• upon necropsy, diseased mice show enlargement and darkening of the liver

cellular
• associated with myocarditis with lymphocytic infiltrates




Genotype
MGI:3687028
cx2
Allelic
Composition
H2-Ab1b-tm1Gru/H2-Ab1b-tm1Gru
Rag1tm1Mom/Rag1tm1Mom
Tg(HLA-DQA1,HLA-DQB1)73Myl/0
Genetic
Background
NOD.Cg-Rag1tm1Mom H2-Ab1b-tm1Gru Tg(HLA-DQA1,HLA-DQB1)73Myl
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
H2-Ab1b-tm1Gru mutation (11 available); any H2-Ab1 mutation (81 available)
Rag1tm1Mom mutation (49 available); any Rag1 mutation (120 available)
Tg(HLA-DQA1,HLA-DQB1)73Myl mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• mice do not develop spontaneous myocarditis like NOD.B6-H2Ab1tm1Gru-Tg(HLA-DQA1,HLA-DQB1)73 mice

immune system
• mice do not develop spontaneous myocarditis like NOD.B6-H2Ab1tm1Gru-Tg(HLA-DQA1,HLA-DQB1)73 mice
• injection of splenocytes from myocarditis-affected donors into healthy transgenic mice results in acute onset of symptoms of severe heart failure 3 weeks post-transfer, reproducing symptoms of the donor mice
• injection of serum from diseased donors with high autoantibody titer does not result in myocarditis





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