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Publication : Genetic control of autoimmune myocarditis mediated by myosin-specific antibodies.

First Author  Kuan AP Year  1999
Journal  Immunogenetics Volume  49
Issue  2 Pages  79-85
PubMed ID  9887344 Mgi Jnum  J:52296
Mgi Id  MGI:1328737 Doi  10.1007/s002510050466
Citation  Kuan AP, et al. (1999) Genetic control of autoimmune myocarditis mediated by myosin-specific antibodies [published erratum appears in Immunogenetics 1999 Jun;49(6):595-6]. Immunogenetics 49(2):79-85
abstractText  Autoimmune disease involves both the development of autoreactivity and the expression of organ damage, and susceptibility is genetically complex. We recently reported that in autoimmune myocarditis susceptibility to antibody-mediated cardiac injury is strain specific. DBA/2 mice develop myocarditis following administration of myosin-specific antibody, while BALB/c mice do not. This susceptibility appears to be controlled by expression of myosin in the myocardial extracellular matrix. CByD2F1 mice are both resistant to induction of myocarditis and do not demonstrate extracellular myosin, indicating a recessive genetic component to these traits. A backcross analysis of susceptibility using DBA/2xCByD2F1 mice revealed a locus on chromosome 12 that is strongly linked with myocarditis. In male mice there was a second region on chromosome 1 that also contributes to disease susceptibility. However, genetic susceptibility in both female and male mice was genetically complex. This study demonstrates that the genetic basis of tissue injury can be analyzed separately from the genetic basis of autoreactivity. Future studies will determine whether the genetic factors identified in this study are also involved in susceptibility to rheumatic fever.
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