IL23A and colitis: Therapeutic approaches that target the pro-inflammatory arm of the immune system by blocking cytokine signalling or by affecting intestinal cell migration are effective in subgroups of patients with IBD.8 Mice that lack IL-23p19 are protected from developing colitis in innate as well as lymphocyte replete models of intestinal inflammation induced by IL-10 signalling defects, bacterial colonisation or innate immune stimulation via the anti-CD40.7 11 These results indicate that IL-10 blockade unleashes an IL-23 mediated immune pathogenesis.