Background & Aims: Mucosal-associated invariant T (MAIT) cells constitute a highly abundant innate-like T-cell population in the human liver that is critical for immune surveillance of hepatic cancers. However, MAIT cells are often dysfunctional in human hepatocellular carcinoma (HCC), for reasons that remain unclear. Here, we aimed to identify the mechanisms driving MAIT cell dysfunction in metabolic dysfunction-associated steatotic liver disease (MASLD), a chronic liver condition that predisposes patients to HCC.
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