Aberrant dendritic cell (DC) presentation of bacterial antigens may contribute to inflammatory bowel disease (IBD) pathogenesis. The balance between effector Th17 cells and FoxP3+ regulatory T cells (Treg) is required the gut homeostasis and depends on DC cues. We reported the increased prevalence of circulating Treg and Th17 in Crohn’s disease (CD) patients compared to healthy controls (HC), yet the role of DC-bacterial interactions are still unclear. Our aim was to assess T cell profiles responding to in vitro DC infection with salmonella in CD patients.
Methods
Monocyte-derived dendritic cells (Mo-DC) were differentiated from peripheral blood of CD (n=13) and HC (n=16) using IL-4/GM-CSF and infected with salmonella Typhimuriumfor 24 hours. The infected Mo-DC were co-cultured with autologous naïve CD4+ T cells for an additional 7-days and T cell polarization assessed using FACS.
Results and conclusions
Mo-DC from CD patients were impaired in their ability to polarize CD4+ T cells towards Th17 and Th1 following salmonella infection compared to that from HC. This suggests an impaired ability to generate robust antibacterial responses in CD patients. Impaired generation of salmonella-specific Th17 by infected DC does not contribute to the increased circulating pan-Th17 in CD patients