Figure 2.

Schematic model of the regulation of intestinal homeostasis by the IL-22/STAT3 pathway in IECs. In the intestine, both innate and adaptive immune cells are capable of producing IL-22 in response to various stimuli. For instance, NKp46+ cells present in the mucosa-associated lymphoid tissue are the major innate source of IL-22. On binding to its heterodimeric receptor complex, IL-22R1 and IL-10R2, IL-22 activates the JAK1 and Tyk2 tyrosine kinases, thus leading to the phosphorylation of STAT3. The active STAT3 then translocates to the nucleus, where it regulates gene expression, which subsequently contributes to the suppression of intestinal inflammation, induces the expression of mucus-associated proteins and the restitution of mucus-producing goblet cells, and enhances the motility of IECs in the process of mucosal wound healing. NK, natural killer; JAK kinases, Janus kinases; IECs, intestinal epithelial cells.