Using a Crohn-like enteritis mouse model, Tuganbaev and colleagues showed that concomitant disruption of the MHC class II-IL10 axis further exacerbates intestinal inflammation.88 These findings suggest that perturbations in the SI microbiota contribute to IBD pathogenesis, in part, through dysregulation of an MHC class II-dependent IL-10 signaling pathway. The gene discussed is IL10; the disease is irritable bowel syndrome.