The adapter TRIF is employed by TLRs 3 and 4 to signal through the TBK1-IRF3/7-IFN-b pathway. There is no previous evidence of an association or functional interaction between TRIF and TLR2. In spite of this, the link between TRIF and the IRF pathway on the one hand, and the unusual employment of TLR2 for signaling to the IFN-b gene in PEM on the other suggested the possibility of a role for TRIF. To test this hypothesis we compared induction of IFN-b expression in wild-type and trif 2/2 PEM or BMM infected with EGDe or DpgdA strains. IFN-b induction strongly decreased in TRIF-deficient macrophages infected with any of the two Listeria strains compared to wild-type PEM, showing the requirement for TRIF (Fig. 3B ). In contrast, BMM showed a TRIF-independent IFN-b production (Fig. S1 ).