As mentioned earlier, IFN-I can promote either health or disease depending on the physiopathological context (Table 2) . Therefore, high level production of IFN-I by pDCs such as occurs during certain herpesvirus infections could contribute to immunosuppression or even lead to immunopathology. Indeed, we have shown that high levels of pDC innate cytokine production during MCMV infection are associated with an ablation of cDCs and a significant delay in the induction of antiviral CD8 T cell responses for up to 48 hours [116] . This transient immunosuppression can be recapitulated by exogenous administration of IFN-I in mouse strains that mount low pDC responses to MCMV infection, pointing to a crucial role of pDC-derived IFN-I in this phenomenon [116] . This impact of pDC functions on the kinetics of induction of antiviral adaptive immunity is striking given the recent observation that better outcomes of early primary viral infection with LCMV in mice or SIV in macaques correlate with increased ratio between antigen-specific CD8 T cells and infected cells in situ very early after challenge [155] . TNF-α has been shown to contribute to the disease induced by MCMV infection, as it contributes to liver pathology independently of NK and T cell responses [156] . pDCs could also contribute to these effects since they are the major source of TNF-α early after infection in different mouse strains [43].