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

Sally Huber1, Wen-Chao Song, Danielle Sartini

  • 1Department of Pathology, University of Vermont, Colchester, Vermont 05446, USA. Sally.Huber@uvm.edu

Viral Immunology
|July 5, 2006
PubMed

Insights

Coxsackievirus B3 infection causes myocarditis via CD1d and Vgamma4 T cells. The decay accelerating factor (DAF) receptor influences this immune response, with its absence altering disease severity and immunopathogenicity.

Area of Science:

  • Immunology
  • Virology
  • Cardiovascular Research

Background:

  • Coxsackievirus B3 (CVB3) infection in BALB/c mice leads to severe myocarditis.
  • Myocarditis initiation involves CD1d upregulation and Vgamma4 T cell activation.
  • A CVB3 mutant with reduced decay accelerating factor (DAF) binding fails to upregulate CD1d or activate Vgamma4+ cells.

Purpose of the Study:

  • To investigate the role of DAF in CD1d expression during CVB3 infection.
  • To determine DAF's role in Vgamma4+ T cell activation during CVB3 infection.
  • To elucidate the immunopathogenicity of viral myocarditis in the absence of DAF.

Main Methods:

  • Infection of BALB/c and BALB/c DAF-/- mice with CVB3.
  • Analysis of CD1d expression levels in infected mice.
  • Quantification of Vgamma4+ T cells and IFNgamma+ cells in spleen.
  • Depletion of Vgamma4+ cells and CD8+ T cells to assess disease protection or aggravation.

Main Results:

  • DAF-/- mice showed modest CD1d upregulation compared to wild-type mice after infection.
  • Despite similar total Vgamma4+ cell numbers, infected DAF-/- mice had fewer Vgamma4+ IFNgamma+ cells.
  • Vgamma4+ cell depletion protected BALB/c mice but not DAF-/- mice from myocarditis.
  • Anti-CD8 depletion protected BALB/c mice but aggravated disease in DAF-/- mice.

Conclusions:

  • DAF plays a role in CD1d expression and Vgamma4+ T cell activation during CVB3 infection.
  • Vgamma4+ T cells are crucial for myocarditis development in wild-type mice but not in DAF-/- mice.
  • The absence of DAF alters the immunopathogenicity of CVB3-induced myocarditis, suggesting differential immune responses.

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