As mentioned above, excessive pDC activation during infections with HIV-1/SIV or with MCMV can lead to an overwhelming production of IFN-I and other innate cytokines. This in turn can lead to immune deregulation, including delaying or disarming of adaptive immunity, or to the generation of a local inflammation which contributes to support viral replication and dissemination [163] . In addition, pDCs have been involved in autoimmune diseases for which certain herpesvirus infections have been suggested to be potential triggers [158, 159] . Thus, the dampening of pDC responses could be a reasonable component of immunotherapeutic strategies aimed at decreasing the immunopathology in these different conditions (Scheme 2). Interestingly, in a model of genital infection of macaques with SIV, the dampening of the pDC response locally in the vagina resulted in reduced local inflammation, including a decreased CD4 T cell infiltration, and led to a significant protection of the animals against repeated high dose challenge with SIV [163] . These effects were achieved by local application of glycerol monolaurate which dampened the activation of endocervical epithelial cells for CCL20 production and therefore prevented the downstream CCR6-dependent recruitment of pDCs in the vagina. Dampening systemic pDC responses in vivo could theoretically be achieved by a number of ways, including treatments with antagonist ligands of the TLR receptors [164] , or the administration of agonistic antibodies to the LILRA4 or CLEC4C receptors which are selectively expressed in pDCs and downmodulate their production of innate cytokines in response to TLR triggering [106] [107] [108] . However, it must be stressed that pDC responses should not be completely switched off, because this may lead to heightened viral replication, as recently demonstrated for inflammatory DCs in the case of a mouse model of intranasal influenza infection. Indeed, in this model, either excessive or absent inflammatory DC responses turned out to be deleterious for the host, due respectively to immunopathology versus loss of control over viral replication. In contrast, dampening of inflammatory DC responses through drug treatment allowed enhanced resistance to disease [165] . Thus, therapies aimed at dampening pDC responses to limit immunopathology in the course of viral infections should be combined with other treatments aimed at controling viral replication, such as antiviral drugs or immunotherapeutic restoration of the cytotoxic antiviral activity of NK cells or CD8 T lymphocytes.