Fig. 4

Inflammatory cytokines and chemokines promoted MAIT cell apoptosis. A Representative dot plot of CCR6 and CXCR6. Comparison of CCR6 and CXCR6 on peripheral mucosal-associated invariant T (MAIT) cells in alcoholic liver disease (n = 18), mixed cirrhosis (n = 19) and healthy control (n = 48). B Representative dot plot of PD-1. Comparison of PD-1 on peripheral MAIT cells in alcoholic liver disease (n = 19), mixed cirrhosis (n = 19) and healthy control (n = 48) (F = 0.816, p = 0.446). C Peripheral blood mononuclear cells (PBMCs) from patients with alcoholic cirrhosis (n = 5) and healthy controls (n = 6) were gated on MAIT cells and then stained with 7-aminoactinomycin D (7-AAD) and Annexin V. Percentage of early apoptotic (7-AAD⁻Annexin V⁺) cells were measured in healthy controls and patients with alcoholic cirrhosis. D Levels of IL-12p40, IL-12p70, and IL-8 were elevated in patients with alcoholic cirrhosis (n = 16) compared with healthy controls (n = 18–24). IL-18 was highly expressed in all groups. E Spearman correlation between MAIT percentage among CD3⁺T cells in patients with alcoholic cirrhosis with IL-8 levels (n = 15); F Representation of gating strategy showing 7-AAD and Annexin V after gating on MAIT cells in PBMCs from healthy humans, which were cultured with 50 ng/ml IL-12 or/ and IL-18 or/and IL-8 for 24 h. Early apoptosis was evidenced by the percentages of 7-AAD⁻Annexin V⁺ cells. Induced apoptosis in MAIT cells after exposure to IL-12, IL-18, and IL-8 stimulation for 24 h (n = 5). Data were analyzed by using the analysis of variance (ANOVA) test, two-sample t-test. (*p < 0.05; **p < 0.01; NS. p > 0.05)