Genetics of Coxsackie B3 (CVB3) myocarditis.
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.
Van Houten
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University of Vermont, Department of Pathology, Burlington 05405.
Huber
S A
SA
D000818:Animals; D003384:Coxsackievirus Infections / Q000276:immunology*; D029822:Enterovirus B, Human; D016219:Immunotherapy, Adoptive; D051379:Mice; D008815:Mice, Inbred Strains; D009205:Myocarditis / Q000276:immunology / Q000382:microbiology*; D016176:T-Lymphocyte Subsets / Q000276:immunology*