To confirm the contribution of LysM positive cells to the type I IFN response against L. monocytogenes as well as to characterize their role during infection with this pathogen, we analyzed homozygous mice, in which the gene encoding IFN-b was cell-specifically deleted on both alleles. As a control, we included IFN-b floxb-luc/floxb-luc mice to demonstrate that the genetic changes in the targeted locus have no impact on their own on the course of infection. C57BL/6, IFNb floxb-luc/floxb-luc , IFN-b floxb-luc/floxb-luc x LysMcre and IFN-b 2/2 mice were infected with Listeria monocytogenes and 24 hours p.i. serum levels of type I IFN were determined by ELISA (Fig. 6A) . Importantly, IFN-b production was identical in C57BL/6 and IFN-b floxb-luc/floxb-luc mice, while the extent of IFN-b expression was dramatically reduced in IFN-b floxb-luc/floxb-luc x LysMcre mice. As a consequence, since type I IFN induction in macrophages depends on feedback signaling, total IFN-a levels were also markedly reduced in IFN-b floxb-luc/floxb-luc x LysMcre mice and they were similar to the levels in IFN-b 2/2 mice (Fig. 6A) .