Induction of IFN-b via TLR2 is no longer an exception. It has recently been shown that vaccinia virus-induced IFN-b production was dependent on TLR2 signaling and it was reported that this was occuring from late endosomes [26] . To investigate if an intracellular localization was also required in the case of Listeria, we pretreated cells with cytochalasin D to prevent internalization and measured IFN-b secretion by macrophages infected with EGDe or the DpgdA mutant (Fig. 5A ). In both cases, IFN-b induction was strongly reduced. Thus, internalization is critical for Listeriamediated IFN-b production. We also used dynasore, a dynamin inhibitor and chloroquine, which inhibits endosome acidification, and measured IFN-b induction in macrophages infected with EGDe or the DpgdA mutant ( Fig. 5B -C). IFN-b synthesis was strongly diminished by both dynasore and chloroquine treatments. Together, these results suggest that the TLR2-dependent IFN-b induction is triggered intracellularly.