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We have observed that lipid accumulation in hepatocytes induces expression of ligands specific to the activating immune receptor NKG2D. Tissue-resident innate-like T cells, most notably \u03b3\u03b4 T cells, are activated through NKG2D and secrete IL-17A. IL-17A licenses hepatocytes to produce chemokines that recruit proinflammatory cells into the liver, which causes NASH and fibrosis. NKG2D-deficient mice did not develop fibrosis in dietary models of NASH and had a decreased incidence of hepatic tumors. The frequency of IL-17A\n            <jats:sup>+<\/jats:sup>\n            \u03b3\u03b4 T cells in the blood of patients with MAFLD correlated directly with liver pathology. Our findings identify a key molecular mechanism through which stressed hepatocytes trigger inflammation in the context of MAFLD.\n          <\/jats:p>","DOI":"10.1126\/sciimmunol.add1599","type":"journal-article","created":{"date-parts":[[2023,9,29]],"date-time":"2023-09-29T17:58:43Z","timestamp":1696010323000},"update-policy":"https:\/\/doi.org\/10.34133\/aaas_crossmark","source":"Crossref","is-referenced-by-count":46,"title":["NKG2D-mediated detection of metabolically stressed hepatocytes by innate-like T cells is essential for initiation of NASH and fibrosis"],"prefix":"10.1126","volume":"8","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-4054-338X","authenticated-orcid":true,"given":"Sonja","family":"Marinovi\u0107","sequence":"first","affiliation":[{"name":"Department of Histology and Embryology, Faculty of Medicine, University of Rijeka, Rijeka, 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