Mucosal-associated invariant T (MAIT) cells represent the most abundant T cell type in human liver. They are characterized by expression of the T cell receptor (TCR) variable subunit Va7.2 together with high expression of CD161. MAIT cells respond to bacterial metabolites presented by MHC-like molecule MR1 on antigen (Ag)-presenting cells (APCs). Accumulating evidence suggests that the gut microbiome (i.e. gut resident bacteria) is involved in the pathogenesis of various liver diseases, especially non-alcoholic fatty liver disease (NAFLD). MAIT cells, by responding to bacterial metabolites, are placed at a central position in the immunological gut-liver axis. A metabolic study in mice suggested that the MAIT cell Ag precursor 5-amino-6-D-ribitylaminouracil (5-A-RU) is able to cross the intestinal barrier to reach both the circulation and the liver. In mouse models, activated liver MAIT cells were recently described as profibrogenic and, similarly, human MAIT cells from patients with liver cirrhosis show a pro-fibrogenic phenotype. It remains poorly understood which cells in the liver are involved in MAIT cell activation, and, consequently, how their profibrogenic function could be prevented.Our aims are to elucidate the role of MAIT cells in selected liver diseases, to identify intrahepatic cellular interaction partners of MAIT cells, and to uncover ways to prevent intrahepatic MAIT cell activation.