Th17 cells have been shown to be potent mediators of IBD in part through production of IL-17 and IFN-γ, and by stimulating myoblasts to secret matrix metalloproteinases (MMPs), which penetrate multiple components of the extracellular matrix leading to epithelial cell damage (54, 55; see ref. 56 for review). Here, IL17A is linked to inflammatory bowel disease.