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1+ T Cells Suppress and V4+ T Cells Promote Susceptibility to Coxsackievirus B3-Induced Myocarditis in Mice1
*
Department of Pathology, University of Vermont, Burlington, VT 05446;
Department of Biology, University of Colorado, Colorado Springs, CO 80933; and
National Jewish Medical and Research Center, Denver, CO 80206
Coxsackievirus B3 infections of C57BL/6 mice, which express the MHC
class II IA but not IE Ag, results in virus replication in the heart
but minimal myocarditis. In contrast, Bl.Tg.E
mice, which are
C57BL/6 mice transgenically induced to express IE Ag, develop
significant myocarditis upon Coxsackievirus B3 infection. Despite this
difference in inflammatory damage, cardiac virus titers are similar
between C57BL/6 and Bl.Tg.E mice. Removing 
T cells from
either strain by genetic manipulation ( knockout(ko)) changes the
disease phenotype. C57BL/6 ko mice show increased myocarditis.
In contrast, Bl.Tg.E ko mice show decreased cardiac
inflammation. Flow cytometry revealed a difference in the cell
subsets in the two strains, with V1 dominating in C57BL/6 mice, and
V4 predominating Bl.Tg.E mice. This suggests that these two
V-defined subsets might have different functions. To test this
possibility, we used mAb injection to deplete each subset. Mice
depleted of V1 cells showed enhanced myocarditis, whereas those
depleted of V4 cells suppressed myocarditis. Adoptively transfusing
enriched V4+ cells to the C57BL/6 and Bl.Tg.E
ko strains confirmed that the V4 subset promoted myocarditis. Th
subset analysis suggests that V1+ cells biased the
CD4+ T cells to a dominant Th2 cell response, whereas
V4+ cells biased CD4+ T cells toward a
dominant Th1 cell response.
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