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Decay-accelerating factor (CD55) promotes CD1d expression and Vgamma4+ T-cell activation in coxsackievirus B3-induced myocarditis.

BALB/c mice infected with the H3 variant of Coxsackievirus B3 (CVB3) develop severe myocarditis which is initiated by up-regulation of CD1d during infection and CD1d-dependent activation of T cells expressing the Vgamma4 T cell receptor. Previous studies have shown that a mutant variant of the H3 virus which shows reduced binding avidity to one of the known CVB3 virus receptors, decay accelerating factor (DAF), fails to up-regulate CD1d or activate Vgamma4+ cells. To determine if DAF has a role in CD1d expression during infection or Vgamma4+ cell activation, BALB/c and BALB/c DAF-/- mice were infected with CVB3. Infected DAF-/- mice show modest increases in CD1d expression compared to infected wild-type BALB/c mice; and although total numbers of Vgamma4+ cells in the spleen are the same as in BALB/c mice, few Vgamma4+ IFNgamma+ cells are detected in infected DAF-/- animals. Vgamma4+ cell depletion protects infected BALB/c mice from myocarditis but does not protect infected DAF-/- animals, indicating that Vgamma4+ cells are not important to disease in these animals. Anti-CD8 depletion of CD8+ T cells protects infected BALB/c mice but aggravates disease in infected DAF-/- animals, indicating that the immunopathogenicity of viral myocarditis differs in the absence of the DAF virus receptor.