Skip to main content
. 2021 Jul 16;22(14):7618. doi: 10.3390/ijms22147618

Figure 5.

Figure 5

ILCs, homeostasis, and inflammatory bowel disease. There are two major subpopulations of ILC1s in the human gut: lamina propria ILC1s (CD161+ CD127+) and intraepithelial ILC1s (NKp44+ CD103+ CD127−). ILC2s are present in lower numbers than ILC1s and ILC3s. ILC2s contribute to epithelial barrier maintenance through the production of IL-13, which promotes the differentiation of intestinal epithelial stem cells toward turf cells and goblet cells. ILC2s also maintain intestinal epithelia homeostasis through the production of amphiregulin (AREG). ILC3s maintain gastrointestinal tract homeostasis by producing IL-22. This cytokine activates intestinal epithelial cells to produce antimicrobial peptides, enhances the renewal of epithelial cells, promotes tissue repair and modulates the homeostasis of adaptive immunity. Alteration of the ILC subset profile disturbs intestinal homeostasis and leads to inflammation in the gut. ILC3s and ILC1s are involved in the induction of inflammation and are closely related to IBD pathogenesis. This conclusion is supported by the amplification of intraepithelial IFN-γ-producing ILC1s in response to IL-12 and IL-15 in the gut of CD patients. This increase is accompanied by a reduction in NCR+ ILC3s, enhancing disease severity.