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. 2017 Apr 6;8:410. doi: 10.3389/fimmu.2017.00410

Figure 1.

Figure 1

Type I interferons (IFN-I) orchestrate a series of intracellular events in immune cells and intestinal epithelial cells (IECs) to cease inflammation resulting in the regeneration of the intestinal epithelium and restoration of the gut barrier. Under normal conditions, low levels of IFN-I are secreted by lamina propria dendritic cells (DCs) and other phagocytes. In response to microbial attack and/or tissue injury, production of IFN-I by these cells is increased that in turn act on T cells to suppress Th17 cell differentiation while promoting Treg expansion thereby limiting inflammation. IFN-I also inhibit the production of pro-inflammatory cytokines (i.e., IL-1β, IL-8, IL-23) and induce the production of anti-inflammatory mediators (IL-1RA, IL-10, IL-27). Furthermore, IFN-I act on IEC and Paneth cells to restrict proliferation and favor their differentiation to establish gut barrier integrity.