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European Heart Journal 1991 12(Supplement D):108-112; doi:10.1093/eurheartj/12.suppl_D.108
Copyright © 1991 by the European Society of Cardiology.
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© 1991 The European Society of Cardiology

Genetics of Coxsackie B3 (CVB3) myocarditis

N. Van Houten and S. A. Huber

University of Vermont, Department of Pathology Burlington, Vermont 05405, U.S.A.

Address for correspondence: Dr S. A. Huber, Department of Pathology, University of Vermont, Burlington, VT, U S.A.

The pathogenic T cell responsible for myocarditis following CVB3 infection differs between BALB/c and DBA/2 mice. Since these two strains are identical at the major histocompatibility (MHC) loci (both H-2d), our aim was to investigate the genetic basis for this difference in T cell immunity, as well as the tissue origin responsible. As previously described, DBA/2 mice are protected from developing myocarditis by CD4+ T cell depletion; BALB/c CUM mice could be protected by CD8+ depletion. TxBM DBA/2 mice were irradiated and reconstituted with thymus and bone marrow cells of either DBA/2 or BALB/c CUM origin. These mice were then tested for susceptibility to CVB3 myocarditis following specific T cell depletion. These studies demonstrated that the pathogenic mechanism is inherent in the bone marrow of the animal and does not reflect thymic selection during T cell ontogeny. Further studies involving C.D2 mice, which are BALB/c AnPt mice congenic with DBA/2, were performed to analyse the susceptibility pattern following specific T cell depletion and virus infection. Analysis of BALB/c AnPt and congenics revealed a pattern consistent with the DBA/2 strain, and not the BALB/c CUM strain. This indicates that the differences in immune pathogenicity lie within subfamilies of BALB/c mice, making information on strain origin important when comparing experimental results in this system.

Key Words: Coxsackievirus B3 • mice • inbred • T lymphocytes • myocarditis


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