Immune dysregulations in alcoholic liver diseases are still unclear, especially regarding alcoholic hepatitis inflammatory burst. Interleukin‐17 (IL‐17) is known to enhance neutrophil recruitment. We studied the IL‐17 pathway in alcoholic cirrhosis and alcoholic hepatitis. Patients with alcoholic liver disease were compared with patients with chronic hepatitis C virus (HCV) infection or autoimmune liver disease and with healthy controls. IL‐17 plasma levels and peripheral blood mononuclear cell secretion were assessed by enzyme‐linked immunosorbent assay (ELISA) and T cell phenotype by flow cytometry. IL‐17 staining and co‐staining with CD3 and myeloperoxidase were performed on liver biopsy specimens. IL‐17 receptor expression was studied on liver biopsies and in human hepatic stellate cells as well as their response to recombinant IL‐17 by chemotaxis assays. IL‐17 plasma levels were dramatically increased in alcoholic liver disease patients. Peripheral blood mononuclear cells of patients with alcoholic liver disease produced higher amounts of IL‐17, and their CD4⁺ T lymphocytes disclosed an IL‐17–secreting phenotype. In the liver, IL‐17–secreting cells contributed to inflammatory infiltrates in alcoholic cirrhosis, and alcoholic hepatitis foci disclosed many IL‐17⁺ cells, including T lymphocytes and neutrophils. In alcoholic liver disease, liver IL‐17⁺ cells infiltrates correlated to model for end‐stage liver disease score, and in alcoholic hepatitis to modified discriminant function. IL‐17 receptor was expressed in alcoholic liver disease by hepatic stellate cells, and these cells recruited neutrophils after IL‐17 stimulation in a dose‐dependent manner through IL‐8 and growth related oncogen α (GRO‐α) secretion in vitro. Conclusion: Human alcoholic liver disease is characterized by the activation of the IL‐17 pathway. In alcoholic hepatitis, liver infiltration with IL‐17–secreting cell infiltrates is a key feature that might contribute to liver neutrophil recruitment. (Clinical trials number NCT00610597). (HEPATOLOGY 2009;49:646–657.)