IL17A and colitis: In this context, T-bet expression in ILCs in the absence of an adaptive immune system works to dampen pro-inflammatory responses, as TRUC mice have been found to develop colitis driven by aberrant numbers of IL-17-producing ILCs.5 By contrast, we now report that in a more physiologically relevant setting, in the presence of an otherwise intact immune system, T-bet deficiency in ILCs results in the development of protective mucosal immune responses.