Given that IL-22-stimulated STAT3 activation in intestinal epithelial cells is critical for mucosal wound healing [59] and that our present study shows that IL-22 attenuated H. pylori-induced CCL20 expression in gastric epithelial cells is mediated by STAT3 activation, it is plausible that the IL-22-STAT3 axis plays a protective role in gastric mucosal inflammation. Here, CCL20 is linked to inflammation.