Although it is unclear as to what factor(s) precisely regulate IL-33 in the gut, it has recently been shown that severe colonic inflammation with a marked increase in IL-33-producing macrophages results after DSS administration to mice expressing a truncated form of the receptor for TGFβ, supporting a pathogenic function for IL-33 during acute colitis and indicates a direct effect of TGFβ on macrophages to limit IL-33 expression[48]. This evidence concerns the gene IL33 and inflammation.