These reversed colitis effects were due to a change in their cytokine environment, with AhR-activated mice having a reduction in the expression of pro-inflammatory mediators; such as IL-6, IL-12, IL-17, IFN-c, MCP-1, exotaxin-1 and TNF-α, but an increase in IL-22 and TGF-β [159,162,163]. Here, AHR is linked to colitis.