The soluble factors produced by pDCs can act in a paracrine manner to recruit other cell types to the site of infection and induce them to produce a second wave of cytokines or chemokines. During MCMV infection, by producing IFN-I and CCL3, pDCs likely contribute to the induction of such a cytokine/chemokine cascade which has been demonstrated to be critical for NK cell recruitment to the sites of viral infection allowing the local delivery of their immunoregulatory and antiviral effector functions [70] . In addition, pDC-derived IL-12 directly induces IFN-γ production by NK cells [13, 22] while pDC-derived IFN-I induces NK cells to proliferate [22] and to acquire cytolytic granules containing perforin and granzyme B, at least in part indirectly by instructing other cell types, most likely cDCs, to produce IL-15 and transpresent it to NK cells in association with the IL-15Rα chain [21, 22, 71, 72] . Upon stimulation with HSV-1, pDCs have been reported to produce IL-18 and thus to most efficiently contribute to induce NK cell IFN-γ production [73] . Human pDCs stimulated with HCMV induce NK cells migration and IFN-γ secretion, but not cytotoxicity [5] which could be consistent with the poor expression of IL-15 by pDCs ( Figure 1 ). More generally, stimulation of pDCs with herpesviruses [69] as well as with other types of viruses including hepatitis C virus [74] or influenza virus [75] induces them to produce a variety of cytokines/chemokines which recruit and activate other innate immune cell types including cDCs, monocytes and NK cells. Finally, pDCs do not contribute to the activation of other innate immune effectors solely by the production of soluble factors but also through cell-cell contacts as illustrated by the demonstration that the ligand for the glucocorticoid-induced tumor necrosis factor receptor-ligand (GITRL) is preferentially expressed on human pDCs upon HSV-1 stimulation and is critical to promote NK cell IFN-γ production and cytotoxicity [76] .