In mice infected with vesicular stomatitis virus (VSV), pDCs have been demonstrated to produce IFN-I in a feedback loop independent manner [96] . The impact of pDC autocrine IFN-I responses has also been studied recently in the context of NDV infection. A crucial role of this positive feedback loop was shown both for sustained IFN-I production by pDCs and for protecting them from productive viral infection [97] . Indeed, in IFNAR -/-pDCs, IFN-I production is poorly sustained and entirely depends on viral replication in the pDCs and the detection of cytoplasmic viral RNA through mitochondrial antiviral signaling protein (MAV)-dependent pathways. Autocrine IFN-I activity has also been shown to protect pDCs from infection by mouse hepatitis virus [79] . Human pDCs are protected from HCMV infection due both to autocrine IFN-I effects and to other yet unidentified mechanisms [6] .