Using real-time RT-PCR we then analyzed the spectrum of IFN-ab genes in wt mice as well as the impact of IFNabR deficiency on their induction. Included were IFN-a2, 4, 5, 6, 9, 11, 12, 13, 14 and IFN-b. All of them were induced in the spleen by Ad3 in vivo and in BMDC in vitro. IFN-ab subtypes were not detectable in the spleen of unstimulated mice or BMDCs (not shown). Fig. 6 shows the patterns of IFN-ab genes induced in vivo and in vitro in the presence or in the absence of IFN-ab feedback signaling. In wt mice and cells IFN-a5 and IFN-b were the most strongly expressed genes and IFN-a13 was the least activated IFNa subtype. IFN-a11 was not induced at all. IFNabR deficiency resulted in an inhibition of IFN-ab gene expression, the strength of which was subtype dependent. In some cases the inhibition was weak (IFN-a2, 4, 5 and IFN-b), in others strong or complete (IFN-a12, 13, and 14) , showing that the expression of different subtypes of IFN-ab are differentially affected by IFN-ab feedback signaling. Collectively, these data show that the adenovirus triggered production of IFN-ab and IL-6 in BMDCs in vitro and in mice in vivo is strongly dependent on intact IFN-ab signaling.