To promote health over disease, antimicrobial immunity must be tightly regulated to allow the mounting of effector responses of sufficient strength and adequate quality for the control of the invading pathogen, but to prevent the development of immunopathology as could result from exacerbated inflammation. This delicate balance can be achieved in part through negative feedback regulatory loops acting at the level of innate immune responses as discussed earlier for pDC activation. Immunoregulatory mechanisms are also in place to finely tune adaptive immune responses, and pDCs have been demonstrated to be able to contribute to this function. In response to EBV stimulation, pDCs can produce anti-inflammatory cytokines such as IL-10 [11] . HSV-1-stimulated pDCs can downmodulate CD4 T cell activation directly through the production of IFN-I and IL-10, and indirectly through the induction of regulatory CD4 T cells, suggesting that pDCs may contribute to prevent excessive, detrimental, adaptive immune responses during viral infections [126] . The coculture of pDCs, but not cDCs, and CD4 T cells in the presence of HCMV leads to the induction of IL-10 producing T cells [127] . pDCs have also been shown able to express the enzyme indoleamine 2,3dioxygenase 1 (IDO), which can induce T cell tolerance through tryptophan catabolism and downstream production of pro-apoptotic metabolites [128, 129] . A role for pDC expression of IDO has been demonstrated in vivo in mice for the generation of an immunosuppressive environment in tumors [130] . In humans, the expression of IDO by pDCs has been proposed to contribute the immune deregulation during HIV-1 infection [131, 132] . However, to the best of our knowledge, there is currently no evidence that IDO can be expressed by pDCs in the course of infections by herpesviruses and that it can play a role in setting the balance between antiviral defense and immunopathology. The addition of an IDO inhibitor in cocultures of HSV-1-stimulated pDCs and CD4 T cells did not prevent the induction of regulatory T cells [126] .