Figure 7.

NK cell-derived IFN-γ alleviates alcohol-induced steatohepatitis through inhibition of IL17A production by ILC1. Female C57BL/6 mice were exposed to CD or ethanol containing diet. Some EtOH-fed mice were injected intravenously with PBS or splenic CD49b⁺NK cells from WT or GKO mice at days 6 and 10 after ethanol feeding (1 × 10⁶ cells each time). The number of liver IL-17A⁺ ILC1 was measured at 6 hours after binge by intracellular staining (n = 4–7/group). (B and C) Frequency or absolute number of liver IFN-γ–producing NK cells (B) or ILC1 (C) in CD- or EtOH-fed mice was shown (n = 8/group). (D–G) EtOH-fed mice were adoptively transferred with PBS or splenic CD49b⁺NK cells from WT or GKO mice at days 6 and 10 after ethanol feeding (2 × 10⁶ cells per mouse). All mice were killed, and liver tissue or plasma was obtained at 6 hours after binge. (D) Plasma concentrations of ALT and AST were measured (n = 4/group). (E) The mRNA level of IL6 and IL1β in liver tissue was detected (n = 4/group). (F) H&E or Oil Red O staining of liver section was performed (scale bars, 100 μm). Representative images are shown (n = 4/group). (G) The percentage and absolute number of hepatic neutrophils were measured by flow cytometry (n = 4/group). One-way analysis of variance was performed in A, D, E, and G. Two-tailed unpaired Student t tests were performed in B and C. ∗P < .05, ∗∗P < .01, ∗∗∗P < .001, ∗∗∗∗P <.0001.