Mice with deletion of MHC II in ILC3 developed intestinal inflammation, arguing that the intestinal selection of T cells is necessary to maintain immune homeostasis at mucosal sites.173,204 Further studies discovered that ILC3s upregulated co-stimulatory molecules such as OX40L after stimulation with TL1A or IL-1β during inflammation and thus promoted colitis via activation of pathogenic T cells.177,205. Here, IL1B is linked to colitis.