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* Department of Pathology, University of Vermont, Burlington, VT 05446; and
Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA 02215
The myocarditic (H3) variant of Coxsackievirus B3 (CVB3) causes severe myocarditis in BALB/c mice and BALB/c mice lacking the invariant J
281 gene, but minimal disease in BALB/c CD1d-/- animals. This indicates that CD1d expression is important in this disease but does not involve the invariant NKT cell often associated with CD1d-restricted immunity. The H3 variant of the virus increases CD1d expression in vitro in neonatal cardiac myocytes whereas a nonmyocarditic (H310A1) variant does not. V
4+ T cells show increased activation in both H3-infected BALB/c and J281-/- mice compared with CD1d-/- animals. The activated BALB/c V4+ T cells from H3-infected mice kill H3-infected BALB/c myocytes and cytotoxicity is blocked with anti-CD1d but not with anti-MHC class I (Kd/Dd) or class II (IA/IE) mAbs. In contrast, H3 virus-infected CD1d-/- myocytes are not killed. These studies demonstrate that CD1d expression is essential for pathogenicity of CVB3-induced myocarditis, that CD1d expression is increased early after infection in vivo in CD1d+ mice infected with the myocarditic but not with the nonmyocarditic CVB3 variant, and that V4+ T cells, which are known to promote myocarditis susceptibility, appear to recognize CD1d expressed by CVB3-infected myocytes.
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