IL17A and inflammatory bowel disease: TNF, an important inflammatory factor involved in the pathogenesis of IBD, not only collaborates with IL-23 to initiate the production of pathogenic IL-17 by ILC3s, but also induces chemokine expression that attracts neutrophils, including CXCL1, CXCL2, and CXCL5, which synergizes with IL-17A to further recruit neutrophils to release tissue damage mediators, resulting in exacerbation of intestinal epithelial cell apoptosis and tissue damage (106).