The entry of effector T cells into a memory stage, however, is accompanied by the ability to rapidly expand their population during recall responses and to down regulate expression of cell surface markers such as CD62L and CCR7 [33] . It was previously reported that primary infection with the wild type Lm induces down regulation of CD62L on the surface of effector CD8 + T cells which reaches its lowest levels at day 8 post-infection [34] . However, over the following weeks, expression of CD62L is up regulated. During recall infection, CD62L is then rapidly down regulated on the surface of memory CD8 + T cells [32, 35] . In order to correlate protection against challenge with Listeria with antigen specific CD8 + T cells, we examined the induction of LLO 91-99 specific CD8 + T cells in response to primary infection with the different Listeria strains. Infection with L.inn::vgc induced a significant population of cytotoxic CD8 + T lymphocytes (Fig. 4B) which, upon challenge with the wild type Lm, showed a CD62L expression pattern similar to that presented in mice primarily infected with the wild type Lm (Fig. 5) . The identity of the memory T-cells induced in response to L.inn::vgc infection was confirmed by testing the CD44 expression on the CD8 + T-cells following recall infection with Lm where high expression of CD44 was observed on CD8 + T-cells derived from mice primarily infected with the recombinant L.inn::vgc strain but not with the wild type L.inn (Fig.  S3) . The inability of the Lm strain lacking listeriolysin O (LLO) [36] as well as the L.inn strain expressing only LLO [37] to induce a protective T cell response reflects the requirement of the entire virulence gene cluster in conferring a long lasting immunity. We therefore show that a non-pathogenic L.inn strain complemented with the entire vgc is capable of inducing a vigorous anti-listerial response.