In humans, pDCs were demonstrated to be the major source of IFN-I production within total peripheral blood mononuclear cells (PBMCs) upon in vitro stimulation with HSV-1 [2] . Indeed, on a per cell basis, purified pDCs produced up to a thousand fold more IFN-I than cDCs or monocytes. Moreover, depletion of pDCs led to over a hundred fold decrease in PBMC production of IFN-I. Resting human pDCs do not contain mRNA for IFN-I. Upon HSV-1 activation, human pDCs rapidly express mRNA of all the IFN-I family members, whereas cDCs do not [38] . Under these conditions, IFN-I mRNA constitute up to 60% of the total pool of pDC neo-synthesized mRNA, attesting to the tremendous energy allocation that pDCs dedicate to the production of these antiviral cytokines upon proper stimulation. Human pDCs also produce high levels of IFN-I in vitro in response to other herpesviruses including HCMV [5] [6] [7] [8] and EBV [11] . In mice, pDCs were likewise demonstrated to be the major source of IFN-I production within total splenic leukocytes upon in vitro stimulation with HSV- 1 [35] or MCMV [39] . Among all the cells producing IFN-I in response to herpesviruses, pDCs are characterized by the fact that their IFN-I production does not require endogenous virus replication [2, 40] . Moreover, pDCs are not productively infected by MCMV [13, 41] or HCMV [6, 7] . However, the resistance of pDCs to herpesvirus infection is not absolute. It depends both on the virus and on the source of pDCs. HHV-6 or HHV-7 productively infect blood pDCs [9, 10] . Tonsil pDCs have been recently reported susceptible to HCMV infection in contrast to blood pDCs [7] .