However the crucial question remained as to whether the L.inn::vgc strain elicits significant adaptive immune responses resembling those of the wild-type strain. Since Lm is located in both phagosomes and cytosol of professional antigen-presenting cells during infection, epitopes derived from Listeria proteins are presented by the MHC pathway thereby priming both effector CD4 + and CD8 + T cells [28, 29] resulting in full elimination of Listeria from the host. Previous experimental studies [30, 31] have revealed that persistence and number of viable microorganisms are important parameters for establishing efficient T cell-mediated immunity. Moreover, it has been shown that the presence of live bacteria in mice organs over the first 48 hours after immunization is critical for the induction of effector CD8 + T cell mechanisms [32] . Indeed we were able to show that all animals immunized with Lm or L.inn::vgc were protected against 206LD 50 of virulent Listeria (Fig. 4A) . Although the L.inn::vgc strain elicits lowered CD4 + mediated inflammatory responses as compared to infection with Lm, it is capable of mounting a successful anti-listerial protective response, indicating that the observed in vivo survival pattern of the L.inn::vgc strain was sufficient to induce protection.