Figure 3.

A schematic overview of the regulatory relationship between DCs and inflammatory bowel disease (IBD). The lost integrity of the epithelial cell barrier and insufficient mucus layer facilitate bacterial translocation to subepithelial regions. Dab2 is expressed by cDCs. The expression of p38α in cDCs regulated the balance between iTreg and Th1 differentiation in a TGF-β2-dependent manner. RA, transforming from dietary vitamin A by RALDH2, induces the release of pro-inflammatory IL-12 and IL-23 by cDCs and promotes intestinal inflammation in the presence of IL-15. pDCs express gut homing receptors, which reside beneath the epithelial layer and are responsible for taking up luminal antigens and gaining the capacity to produce IL-6 and IL-8 TNF-α, which plays a key role in the establishment of IBD in model rats.5.2. Intestinal Tumors and DCs.