pDCs do not contribute to the production of type I IFN during Listeria monocytogenes infection In response to a wide variety of enveloped DNA and RNA viruses (e.g., Influenza virus, vesicular stomatitis virus) as well as parasites (Plasmodium falciparum) and CpG oligonucleotides, IFN type I is produced by pDCs [35] . L. monocytogenes was shown after intragastric administration to activate pDCs in spleen and in mesenteric lymph nodes as detected by an increased expression of MHC II and CD86 [36] . By extrapolation, a contribution of pDC to the type I IFN response after systemic Listeria infection could be expected, although in vitro stimulation of splenic pDC with Listeria did not induce type I IFN [28] . To evaluate the contribution of pDC to the overall IFN production in vivo after Listeria monocytogenes infection, we performed depletion experiments. To this end, 24 hours prior to infection mice were intravenously injected with the depleting antibody anti-mPDCA-1. 24 hours p.i. spleens were analyzed for the presence of pDCs. Figure 4A demonstrates gating strategy for pDCs and depletion efficiency.