Infection with Listeria monocytogenes shows an early stage of lymphocyte apoptosis. This is an obligatory stage the extent of which depends on infective dose. Lymphocyte apoptosis occurs early and is rapidly superseded, yet it has a strong biological consequence. The immunological effect of lymphocyte apoptosis following infection is increased susceptibility to L. monocytogenes infection due, in part, to upregulation of IL-10 on macrophages and DC. Lymphocyte apoptosis is dependent on bacterial expression of the pore-forming toxin listeriolysin O (LLO). Also, purified LLO can lead to the induction of death pathways similar to infection, demonstrating that it is a killer agent generated by L. monocytogenes. Signaling through the type I interferon receptor potentiates cell death induced by the bacteria or LLO. Infection with L. monocytogenes also causes death of phagocytic cells, the nature and significance of which is not clear at present. Infection with L. monocytogenes is a tractable model to examine pathogen-induced cell death pathways and their possible immunological consequences in multiple cell types following infection.