Fig 1: Severe imbalance in ratio of liver ILC1 to NK cells during chronic alcohol abuse. (A) Female C57BL/6 mice were exposed to the Gao-Binge model with 10-day chronic ethanol feeding plus 1 binge. Liver mononuclear cells were isolated from the mice fed with liquid diet containing ethanol at 5% (v/v) (EtOH) or pair-fed control diet (CD). Percentage and absolute number of group 1 ILCs (CD45+CD3-NK1.1+ cells) were measured by flow cytometry (n = 6–7/group). (B and C) Expression of TRAIL (B) and CD69 (C) on hepatic group 1 ILCs from CD- or ethanol-fed mice were examined by flow cytometry (n = 7–8/group). (D) Expression of T-bet, Eomes, and ROR?t on liver ILC1 (CD45+CD3-NK1.1+CD49b-CD49a+) and NK cells (CD45+CD3-NK1.1+CD49b+CD49a-) from ethanol-fed mice was shown. (E) The numbers of liver ILC1 and NK cells from CD- or EtOH-fed mice were measured, and the ratios of ILC1 to NK cells were shown (n = 6/group). (F) Male C57BL/6 mice were exposed to the Gao-Binge model with 10-day chronic ethanol feeding plus 1 binge or control diet. The ratio of liver ILC1 to NK cells was shown (n = 3–4/group). (G) Female C57BL/6 mice were exposed to CD, chronic ethanol consumption for 5 days, 10 days, 10 days plus binge, or binge only. The ratios of liver ILC1 to NK cells were shown (n = 4/group). Two-tailed unpaired Student t test was performed in A–C, E, and F. One-way analysis of variance was performed in G. ns, no statistical significance. *P < .05, **P < .01, ***P < .001, ****P <.0001.