In variance to our data, pDCs and various types of non-pDCs [10, 42] were suggested to be responsible for the type I IFN responses to adenoviral vectors in mice. In [10] the loss of TLR9 signaling resulted in a reduction of the IFN-a response in mice infected with the recombinant species C Ad-lacZ [10] . This finding suggested a significant contribution of TLR9, and therefore of pDCs, to the Ad-induced IFN-ab response in vivo. The ratio of pDCs to mDCs (approximately 1:1) in the spleen of animals used in the above study was quite different from that we and others [50] have found (approximately 1:10). This may explain the conflicting results on the role of TLR9 in vivo, between this previous study and ours. In another study [42] the induction of IFN-ab was studied in mice with an artificially enlarged pool of DCs (due to prior pretreatment with sFLT-3L), 24 h after recombinant Ad administration. In our study naïve mice were used and 24 h after Ad infection the levels of IFN-ab were already below the detection limit. Of note also, the bone marrow stromal antigen 2 (BST2) (that is recognized by the PDCA-1 antibody used for isolation of pDCs in [42] ), was shown to be up-regulated on numerous cell types following stimulation that triggers an IFN response [81] . Thus, the use of the PDCA-1 antibody for the isolation of pDCs seems to be more reliable in the case of uninfected mice [81] .