Subsequently, impaired DC activation led to the generation of defective virus-specific CD8+ T cells that displayed a dysfunctional effector phenotype characterized by low KLRG-1, low CXCR3 expression, reduced IFN-γ and high IL-10 production at the peak of infection that hindered the control of the viral clearance at the peak of the infection. Here, CXCR3 is linked to infection.