Thus, blockade of type I IFN signaling at day 4 after infection resulted in a distinct antigen-presenting cell activation phenotype compared to MAR1-5A3 treatment at day 2; this suggests that disruption of type I IFN signaling pathways at particular stages of infection might limit the ability of antigen-presenting cells to provide key temporal signals that allow optimal generation of antigen-specific effector CD8+ T cells. This evidence concerns the gene CD8A and infection.