NCR1 and Yersinia enterocolitica infectious disease: This is consistent with a previous study suggesting that NCR− ILCs have a potency to produce more IFNγ than NCR+ ILCs in the gut during Yersinia enterocolitica infection.53 NCR expression in intestinal ILCs is not stable, as some ILCs downregulate NCRs during differentiation, to become double-negative for NK1.1 and NCR.33 Our fate-mapping analysis suggests that while the majority of IFNγ-producing ILCs originate from NKp46+ cells in the colon of uninfected mice, C. jejuni infection induces IFNγ production predominantly by ILCs that derive from distinct NKp46− progenitor cells.