CCR6 and colitis: The absence of ILC1s in T-bet−/− mice is linked to increased susceptibility to enteric infections.2,6,12–14 We have previously reported the phenotype of TRUC mice that develop spontaneous colitis, which is dependent on IL-17-producing CCR6+ ILC3s in the absence of adaptive immunity.5 Increased frequency of inflammatory ILC1s has also been found in inflamed intestine from Crohn’s disease patients.6,13,15 However, whether T-bet expression in ILCs drives protective or pathogenic mucosal immune responses in the presence of an intact immune system still needs to be elucidated.