Engagement of TLRs by various microbe-associated molecular patterns induces activation and translocation to the nucleus of NF-kB, IRF3, IRF7 and/or activator protein-1 (AP-1), which collaborate to induce transcription of type I IFNs [37] . We addressed the role of these transcriptional activators in the IFN-b response to wild-type Listeria and DpgdA, and revealed that inactivation of IRF3 totally abrogated this response to both strains while IFN-b induction was significantly but not totally impaired in IRF7-deficient macrophages, indicating that both of these transcription factors are required for induction of IFN-b following infection with L. monocytogenes. We also assessed the involvement of NF-kB in this response using induction of the IkB gene as a readout. We observed an induction of IkB expression in macrophages which was similar after infection with EGDe or DpgdA. Thus, activation of NF-kB by Listeria is independent of PgdA, strongly suggesting that the elevated IFN-b production by the DpgdA mutant mostly relies on IRF3.