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While immune responses have been rigorously examined after intravenous  Listeria monocytogenes  ( Lm ) infection, less is understood about its dissemination from the intestines or the induction of adaptive immunity after more physiologic models of foodborne infection. Consequently, this study focused on early events in the intestinal mucosa and draining mesenteric lymph nodes (MLN) using foodborne infection of mice with  Lm  modified to invade murine intestinal epithelium (InlA M   Lm) . InlA M   Lm  trafficked intracellularly from the intestines to the MLN and were associated with Batf3-independent dendritic cells (DC) in the lymphatics. Consistent with this, InlA M   Lm  initially disseminated from the gut to the MLN normally in  Batf3  –/–  mice. Activated migratory DC accumulated in the MLN by 3 days post-infection and surrounded foci of InlA M   Lm . At this time  Batf3  –/–  mice displayed reduced InlA M   Lm  burdens, implicating cDC1 in maximal bacterial accumulation in the MLN.  Batf3  –/–  mice also exhibited profound defects in the induction and gut-homing of InlA M   Lm -specific effector CD8 T cells. Restoration of pathogen burden did not rescue antigen-specific CD8 T cell responses in  Batf3  –/–  mice, indicating a critical role for  Batf3  in generating anti-InlA M   Lm  immunity following foodborne infection. Collectively, these data suggest that DC play diverse, dynamic roles in the early events following foodborne InlA M   Lm  infection and in driving the establishment of intestinal  Lm -specific effector T cells.

Mucosal CD8 T Cell Responses Are Shaped by Batf3-DC After Foodborne Listeria monocytogenes Infection