Our data indicate that efficient NK cell activity contributes to the adaptive arm of the immune response to MCMV by promoting the accelerated expansion of antigen-specific CD8 T cells. Like the contribution NK cells make to the maintenance of the cDC compartment, our data support a role for NK cell control of pDC IFN-a/b production for the promotion of antigen-specific CD8 T cell expansion. IFN-a/b can have both positive and negative effects on CD8 T cell responses [20, 21, [51] [52] [53] . For example, the optimal expansion of CD8 T cells in response to LCMV infection has been demonstrated to be dependent on the ability of the CD8 T cell compartment to receive IFN-a/b-mediated signals [53] . However, within the same viral system, IFN-a/b also drives the early attrition of both antigen-specific and bystander CD8 T cell populations [20, 21] . Here, we show that the delay in the expansion of antiviral effector CD8 T cells in the absence of an efficient NK cell response to MCMV occurs within the context of excessive production of IFN-a/b by pDCs. Moreover, we demonstrate that exogenous administration of IFN-a can override the ability of efficient NK cell activity to promote the accelerated expansion of functional antiviral CD8 T cells. The IFN-a-mediated effects on CD8 T cell expansion could be direct or a downstream consequence of the loss of cDCs. However, our results suggest a direct activity of IFN-a/b on CD8 T cells, as the administration of IFN-a leads to the complete disappearance of early antiviral CD8 T cells but only to an incomplete decrease in cDC numbers.