Successful treatment of chronic inflammatory diseases integrates both the cessation of
inflammation and the induction of adequate tissue repair processes. Strikingly, targeting a
single proinflammatory cytokine, tumor necrosis factor (TNF), induces both processes in a
relevant cohort of inflammatory bowel disease (IBD) patients. However, the molecular
mechanisms underlying intestinal repair following TNF blockade during IBD remain elusive.
Using a novel humanized model of experimental colitis, we demonstrate that TNF interfered …