OC-029 Phenotype of Human Intrahepatic Innate Lymphoid Cell Subsets in Heatlh and Disease

Introduction Innate lymphoid cells (ILCs) involve in the initiation, regulation and resolution of inflammation. Although the role of ILCs in murine liver fibrosis and biliary proliferation has been reported, the phenotypic characteristics and functional role of these cells in human liver disease remains undefined. We explored the detailed phenotype of human intrahepatic ILCs to gain insight on their function. Methods Liver infiltrating lymphocytes from normal liver tissue, autoimmune liver diseases (AILD), alcoholic liver disease (ALD) and non-alcoholic steatohepatitis (NASH) explants were phenotyped with flow cytometry. Results Total intrahepatic ILC (CD3 − lineage − CD45 − CD127 + ) comprised 1% (IQR 0.4–1.7%) of the CD3 − CD45 + population in normal liver and 0.4% for ALD/NASH and autoimmune livers. The ILC1 subset constituted the majority of intrahepatic ILC and its frequency is higher in normal liver compared to diseased livers (85% vs. 67%) (p + CRTH2 + ILC2 subset and ILC3 subset frequency are higher in diseased livers compared to normal livers. Interestingly, frequency of ILC3 is significantly higher in ALD compared to normal liver (p 90%). Of likely functional importance, intrahepatic ILC1 expressed IFN-γ (40%) while ILC2 expressed IL-13 (20–50%) in diseased states. Conclusion We report for the first time the presence of all three ILC subsets within the human liver immune cell infiltrates. CXCR3 + IFN-γ expressing ILC1 subset is enriched in both normal and inflamed diseased livers. Higher frequencies of CCR6 + VLA5 + VLA6 + IL-13 expressing ILC2 are observed in diseased livers suggesting that this subset may play a role in biliary pathology and peri-biliary fibrosis. Disclosure of Interest None Declared