In particular, the ensemble of our data unravel a new scenario in which IFN-α, cytokines produced early in response to viral infections or other danger signals, can rapidly induce a polyfunctional DC type, i.e. the in vivo counterpart of IFN-DC, capable of secreting IL-12, IL-1β and IL-23 and concomitantly inducing the emergence of Th1, Th17 and Th1/Th17 CD4 T cells. Here, IFNA1 is linked to viral infectious disease.