The lack or low level of replication of certain herpesviruses and other viruses in pDCs may seem surprising considering the ability of many of these viruses to productively infect cDCs. The mechanisms that protect pDCs from productive viral infection are not entirely understood. However, autocrine IFN-I responses certainly play an important role as we initially reported by showing over a ten-fold increased proportion of infected pDCs in IFNAR -/versus WT mice challenged with an EGFPexpressing MCMV [13] . In these experimental settings, the ability to respond to IFN-I did not only protect pDCs from viral infection but also further enhanced their ability to produce IFN-I by about four-fold [12] . However, a significant production of IFN-I by pDCs still occurred in IFNAR -/animals.