Interleukin-23 and Th17 Cells in the Control of Gut Inflammation

Figure 1

Role of Th17 cells in the modulation of intestinal inflammation. Th17 cells differentiate from naïve T lymphocytes under the stimulus of TGF-𝛽, IL-6, and IL-1, while the dendritic cells derived IL-23 and the Th17 cell-derived IL-21 contribute to maintain/expand Th17 cell populations. Th17-derived cytokines, such as IL-17A, IL-21, and IL-22, promote the recruitment of inflammatory cells in the intestinal lamina propria, due to their ability to enhance the synthesis of chemoattractants and adhesion molecules (e.g., ICAM-1) by epithelial and endothelial cells, respectively. IL-17A, IL-21, and IL-22 stimulate fibroblasts to make matrix metalloproteinases, a family of enzymes that could contribute to the tissue damage and remodeling occurring in IBD. IL-17A and IL-22 also stimulate the synthesis of antibacterial proteins, including defensins, by epithelial cells. DC; Dendritic cells; TGF𝛽; transforming growth factor-𝛽; MMPs; matrix metalloproteinases; ICAM-1; intercellular adhesion molecule-1.