Macrophages have been identified as one of the target cell population in the murine spleen [26] . Besides, macrophages play a major role in the early innate defense against Listeria monocytogenes via secretion of different cytokines [20, 56] . However, DCs were also observed to be directly infected by L. monocytogenes [57] . Since IFN induction requires intracellular Listeria, we would have expected that DCs, in addition to monocytes/macrophages, would be involved in IFN-b production. This is apparently not the case, because i) only negligible amounts of IFN-b are produced in infected mice, in which IFN-b is conditionally deleted by LysMcre. This also excludes a major contribution of a non-lymphoid tissue associated cell. ii) Similar amounts of reporter luciferase are produced in the global reporter mice and in the mice reporting production of IFN-b by monocytes/macrophages and neutrophilic granulocytes. Although LysMcre is supposed to be expressed by a small population of DCs [44] , CD11ccre mice experiments confirm that conventional DCs do not significantly contribute to IFN-b production. We also could exclude the contribution of pDC. The depletion of this cell population had no effect on the overall production of type I IFN. This extends the in vitro data of Stockinger et al. [28] to the in vivo situation. Finally, the involvement of neutrophils that are expressing LysMcre was also excluded by a depletion experiment.