Using this system, we were able to design a doxycycline treatment protocol which, in BALB/c mice, closely mimics the extent and the kinetics of efficient NK cell-mediated control of viral replication observed in Klra8. Indeed, under the experimental conditions selected, the viral burdens in Klra8 mice and in DN-SCP-MCMV-infected, doxycycline-treated BALB/c mice were comparable at the different time points examined, and much lower than in untreated DN-SCP-MCMV-infected BALB/c animals ( Figure 7A ). The reduction in viral burden in doxycycline-treated DN-SCP-MCMVinfected BALB/c animals led to a significant, strong decrease in the serum levels of the pDC-derived cytokines IFN-a and IL-12p70 ( Figure 7B ) and allowed the maintenance of cDCs ( Figure 7C ). Moreover, we observed an accelerated activation Figure  7D ). The treatment of DN-SCP-MCMV-infected Klra8 mice with doxycycline had no effect on any of the parameters tested (unpublished data). Thus, our data indicate that, in Klra8 mice, the ability of NK cells to dampen innate cytokine production by pDCs and thus to promote optimal conditions for the initiation of antiviral cDC and CD8 T cell responses result from their exquisite capacity to control viral replication early and efficiently after infection.