To examine the role of TLR3, which uses TRIF to trigger IFNb synthesis, we compared induction of IFN-b in wild-type and tlr3 2/2 PEM infected with EGDe or DpgdA strains. IFN-b production was decreased in TLR3-deficient PEM infected with EGDe or DpgdA (Fig. 4A) . We also compared induction of IFN-b in wild-type and tlr4 2/2 PEM infected with EGDe or DpgdA strains, as TLR4 can mediate TRIF-dependent synthesis of IFN-b. In contrast to TLR3-deficient PEM, TLR4-deficient PEM did not show a decrease in IFN-b response to EGDe or DpgdA (Fig. 4B ). Thus, IFN-b induction in response to Listeria infection relies in part on TLR3 and does not require TLR4.