Abstract
While the intestinal immune system coexists[DPM1] with commensal bacterial flora through immunological tolerance, invading microorganisms are recognized and properly eliminated. However, it remains unknown what kinds of cells in the intestine initiate immune responses and how they activate host immunity. Recently, we identified a subset of CD11chiCD11bhi lamina propria (LP) dendritic cells (DCs) as TLR5-expressing cells, which have the ability to activate adaptive immune responses. The LPDCs induced antigen-specific Th17 cells as well as Th1 cells in a TLR5-dependent manner. In addition, they acted on naïve B cells to induce their development to immunoglobulin A (IgA)+ plasma cells in response to flagellin, and such IgA+ plasma cell generation took place in a gut-associated lymphoid tissue (GALT)-independent fashion. Our findings demonstrate unique properties of LPDCs and the importance of TLR5 for adaptive immunity in the intestine. We also generated and examined mutant mice of ATG16L1. ATG16L1 is a component of autophagy machinery and has been reported to be a candidate gene responsible for susceptibility to Crohn's disease. We discuss a novel role for autophagy in the regulation of the inflammatory immune responses in the intestine.
