{
  "abstract": "Hepatocellular carcinoma (HCC) is the third most common cause of cancer-related mortality worldwide and a tumour with robust molecular subtypes including hepatocyte-like, cholangiocyte-like and progenitor-like1 tumours. HCC development is primarily driven by chronic hepatitis and cirrhosis, and its microenvironment possesses a highly variable immunogenicity.2 HCC can be divided into (i) an inflamed (35%) and (ii) a non-inflamed class (65%) with activated, exhausted or immune-like (inflamed class) or intermediate and excluded groups (non-inflamed class),3 while many T cell-infiltrated HCC feature an accumulation of dysfunctional exhausted CD8+T cells.45 Accumulation of more functional tissue-resident memory-like T cell responses has been associated with viral aetiology of HCC, an entity with slightly higher response rates to immune checkpoint inhibition.6 7 Preclinical models of metabolic dysfunction-associated steatohepatitis (MASH)-driven HCC also indicate that CD8+T cells can be drivers of hepatocarcinogenesis through the secretion and activity of different pro-inflammatory cytokines (eg, IL-15), likely associated with the lipid accumulation in MASH.7 8 However, the mechanisms that determine T cell dysfunction in MASH-HCC have remained incompletely understood.",
  "authors": [
    {
      "affiliations": [
        "Division of Chronic Inflammation and Cancer, Deutsches Krebsforschungszentrum, Heidelberg, Baden-Württemberg, Germany",
        "The M3 Research Center, Tübingen, Germany"
      ],
      "name": "Mathias F Heikenwälder"
    },
    {
      "affiliations": [
        "Clinic for Internal Medicine II, Gastroenterology, Hepatology, Endocrinology and Infectious Disease, Medical Center-University of Freiburg, Faculty of Medicine, University of Freiburg, Freiburg, Germany"
      ],
      "name": "Bertram Bengsch"
    }
  ],
  "title": "12-HETE: a novel lipid mediator of CD8+ T cell dysfunction in MASH/HCC",
  "uid": "d55b7272-95a9-5604-a839-0dfdff165188"
}