IL-33-deficiency has been reported to protect mice from dextran sulfate sodium (DSS)-induced experimental colitis by inhibiting Th17 cell responses [138], and the IL-33/ST2 axis controls Th17 immune responses that exacerbate allergic airway disease, thus implicating IL-33 as an important therapeutic target for autoimmune diseases [139]. This evidence concerns the gene IL33 and colitis.