Analysis Tools
cardiovascular system
| N |
• animals have normal sized hearts, normal ECG, and show no sign of autoimmune pathology
|
|
• recipient animals develop cardiomegaly by 12 weeks after transfer
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• mice receiving splenic lymphocytes from animals with heart block display first-degree heart block as early as 2 weeks after transfer, with 50% progressing to complete heart block in 8 weeks
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• recipient animals develop mononuclear cell infiltrates within heart wall by 12 weeks after transplant
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myocarditis
(
J:113267
)
|
• when young mice receive splenic lymphocytes from older NOD.DQ8/H2Ab-1 mice with heart block, myocarditis is triggered in 100% of recipients
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immune system
|
• recipient animals develop mononuclear cell infiltrates within heart wall by 12 weeks after transplant
|
myocarditis
(
J:113267
)
|
• when young mice receive splenic lymphocytes from older NOD.DQ8/H2Ab-1 mice with heart block, myocarditis is triggered in 100% of recipients
|
|
• anticardiac myosin autoantibodies reach a titer of 1:10000 in recipient mice at 12 weeks posttransfer
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• younger mice receiving splenic lymphocytes from older DQ8 transgenic, H2-Ab1-null mice with heart block develop heart block, myocarditis, and autoantibodies
• when younger mice receive serum from the same older animals, no cardiac pathology is observed
• recipient mice receiving CD4 T cells from older donor animals with heart block develop heart block as early as 4 weeks posttransfer; all animals are diseased by 12 weeks and upon necropsy, heart are enlarged
• mononuclear cells are more numerous and infiltrates more widespread than in animals that receive total splenocytes (containing CD4 T cells) in the myocardium
• disease onset is somewhat accelerated compared to recipients receiving total lymphocytes;
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growth/size/body
|
• recipient animals develop cardiomegaly by 12 weeks after transfer
|
