(A) Localization. During homeostasis, NK cells are primarily circulating cells transiting through the vasculature whereas ILC1s are resident within tissue. During inflammation, ILC1 residency is maintained, and NK cells may also be recruited into the tissue.
(B) Phenotype. Mouse NK cells and ILC1s both express the activating NK cell receptors NKp46 and NK1.1 as well as the transcription factor T-bet. Only NK cells express and require Eomes for their development, and bear activating Ly49 receptors, CD11b, and CD49b on their surface. In contrast, ILC1s develop independently of Eomes, and can be characterized by expression of CD200r1 and a distinct integrin profile, including CD49a and CD61. CXCR6 expression is unique to hepatic ILC1s. NK cells and ILC1s are stable cell lineages during homeostasis and MCMV infection, although NK cells have been observed to adopt an ILC1-like phenotype in various cancer models.
(C) Function. ILC1s are thought to be less cytotoxic than NK cells, and may mediate cytotoxicity through a distinct set of effector molecules (e.g. TRAIL). However, ILC1s are potent and early IFN-γ-producing cells in response to cytokine stimulation.