pDCs isolated from MCMV-infected animals up-regulate CD80, CD86, CD40 as well as MHC molecules and efficiently prime naive CD8 T cells in vitro for proliferation and IFN-γ production, when pulsed with exogenous antigens [13] . However, neither the ability of pDCs to naturally process and present MCMV antigens, nor the role of pDCs in the global shaping of antiviral CD8 T cells responses, have been addressed during the course of MCMV infection. During MCMV infection, pDC IFN-I production was required to promote cDC maturation and thus likely helped the induction of antiviral adaptive cellular immune response [13] . pDCs exposed in vitro to HSV-2 induced T cell proliferation, more strongly for CD8 T lymphocytes [4] . pDCs isolated from the draining lymph nodes of HSV-1-infected mice had only a poor ability to induce IFN-γ production by HSV-specific CD4 and CD8 T cells as compared to cDCs [123, 124] , suggesting that pDCs did not have a major role in the direct priming of T lymphocytes during HSV-1 infection. However, in these experimental settings, pDCs promoted optimal functions of cDCs via cell-to-cell contacts involving CD2 and CD40L, which contributed to enhance HSV-1-specific CD8 T cell responses [123] . Finally, in vitro stimulation of pDCs with HCMV or influenza promoted B cell activation and their differentiation into specific antibody-secreting plasma cells, through IFN-I-and IL-6-dependent effects [8, 125] .