The intravenous infection of mice with another herpesvirus, HSV-2, also leads to a systemic IFN-I production that is abrogated upon anti-BST2 antibody-mediated pDC depletion [3] . Thus, no doubt remains that splenic pDCs are the major source of IFN-I during systemic infections of mice with several herpesviruses in vivo. Interestingly, an intra-vaginal challenge with HSV-2 also leads to a pDC-dependent IFN-I production, but only locally as the cytokines can be detected in the vaginal wash but not in the blood, consistent with the lack of dissemination of the infection in immunocompetent animals [46] .