The unique ability of pDCs to produce very high levels of all subtypes of IFN-I in response to herpesvirus infections cannot be solely explained by their expression of TLR9 and by their ability to engulf viral particles or infected cells. Indeed, these two properties are shared with cDCs, especially the CD8α subset in the mouse, which still does not produce significant levels of IFN-I under the same experimental conditions. Indeed, additional properties have been demonstrated to contribute to the exquisite ability of pDCs to produce high levels of IFN-I upon viral stimulations (Scheme 1).