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Abstract
Listeria monocytogenes (Lm) infection induces robust CD8 T cell responses, which play a critical role in resolving Lm during primary infection and provide protective immunity to re-infections. Comprehensive studies have been conducted to delineate the CD8 T cell response after Lm infection. In this review, the generation of the CD8 T cell response to Lm infection will be discussed. The role of dendritic cell subsets in acquiring and presenting Lm antigens to CD8 T cells and the events that occur during T cell priming and activation will be addressed. CD8 T cell expansion, differentiation and contraction as well as the signals that regulate these processes during Lm infection will be explored. Finally, the formation of memory CD8 T cell subsets in the circulation and in the intestine will be analyzed. Recently, the study of CD8 T cell responses to Lm infection has begun to shift focus from the intravenous infection model to a natural oral infection model as the humanized mouse and murinized Lm have become readily available. Recent findings in the generation of CD8 T cell responses to oral infection using murinized Lm will be explored throughout the review. Finally, CD8 T cell-mediated protective immunity against Lm infection and the use of Lm as a vaccine vector for cancer immunotherapy will be highlighted. Overall, this review will provide detailed knowledge on the biology of CD8 T cell responses after Lm infection that may shed light on improving rational vaccine design.
Highlights
Listeria monocytogenes (Lm) is a Gram-positive, facultatively anaerobic intracellular bacterium that can cause listeriosis
But lower IFN-γ, tumor necrosis factor (TNF)-α and IL-2 compared to memory CD8 T cells in the spleen [107,145], suggesting functional tailoring to the unique tissue environment that may influence their contribution to protective immunity
CD8 T cell response and the availability of immunological tools developed in the past decades
Summary
Listeria monocytogenes (Lm) is a Gram-positive, facultatively anaerobic intracellular bacterium that can cause listeriosis. DC at eliciting CD8 T cell responses to Lm [26] In addition to their role in transporting Lm to the T cell zone and activating CD8 T cells, a new study demonstrated that Batf3-dependent CD8α+ DC are a vital source of IL-18, which subsequently licenses Natural Killer (NK) cells to produce IL-10 [27]. As NK cell-derived IL-10 promotes susceptibility to Lm infection [28], this new study provides an additional mechanism that contributes to the resistance of mice deficient in Batf3-dependent CD8α+. Lm invades the gut epithelium and disseminates to the draining mesenteric lymph nodes (MLN), a primary site of T cell priming in response to intestinal pathogens. Further work needs to determine whether the acquisition and transit of Lm is uncoupled from T cell priming, in which case one DC subset may acquire and transport Lm to the MLN and another DC subset may prime T cells and generate gut-tropic effector CD8 T cells after oral
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