Key result
During Coxsackievirus B3 infection in mice, Vgamma1+ T cells promote humoral immunity and protection, whereas Vgamma4+ T cells are pathogenic and increase myocarditis susceptibility.
Why the study?
Do Vgamma1+ and Vgamma4+ T cells have different functions in Coxsackievirus B3-induced myocarditis in mice?
Do Vgamma1+ and Vgamma4+ T cells have different functions in Coxsackievirus B3-induced myocarditis in mice?
In a murine model of Coxsackievirus B3 myocarditis, Vgamma1+ T cells promote protective humoral immunity while Vgamma4+ T cells drive pathogenesis.
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Animal data on opposing γδ T-cell roles in CVB3 myocarditis should not change practice; leaves open human validation.
Huber et al. (2005) studied Coxsackievirus B3 infection and myocarditis. Antibody depletion of Vgamma1+ or Vgamma4+ cells; exogenous recombinant IFNgamma was evaluated on Myocarditis susceptibility and virus neutralizing antibody response. During Coxsackievirus B3 infection in mice, Vgamma1+ T cells promote humoral immunity and protection, whereas Vgamma4+ T cells are pathogenic and increase myocarditis susceptibility.
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