More than that, in a dextran sulfate sodium colitis mouse model, blocking of IL-17 activity results enhanced the expression of tumor necrosis factor (TNF)-α, interferon (IFN)-γ and IL-6, and the infiltration of T cells (CD4+ Th cells) and granulocytes–monocytes in the gut mucosa, finally resulting in the progression of colitis. Here, IL17A is linked to colitis.