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Shall we blame CD4 T cells for everything?
  1. Tim F Greten,
  2. Firouzeh Korangy
  1. Gastrointestinal Malignancy Section, Thoracic and Gastrointestinal Oncology Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA
  1. Correspondence to
    Professor Tim F Greten, Thoracic and GI Oncology Section, Thoracic and Gastrointestinal Oncology Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, NIH/NCI/CCR Building 10, Rm 12N226, 9000 Rockville Pike, Bethesda, MD 20892, USA; tim.greten{at}nih.gov

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Persistent inflammatory conditions in the liver promote chronic liver damage and liver fibrosis ultimately leading to hepatocellular carcinoma (HCC). Multiple cytokines have been investigated in the context of acute and chronic liver damage. Interleukin 17 (IL-17) is a proinflammatory cytokine produced by a subset of CD4 T cells (T helper 17 (Th17) cells). IL-17 recruits other immune cells such as monocytes and neutrophils to the site of inflammation in response to invasion by pathogens. It can promote inflammation and has been linked to various autoimmune disorders.1 In the liver, Th17 responses have been shown in non-alcoholic steatohepatitis, cholestatic liver diseases, liver fibrosis and antimicrobial defences.2 In this issue, Nadine Kuttkat from the Trautwein group investigated Th17 cells in a murine model of liver injury and HCC development.3 Following a previous report on the role of nuclear factor-kappa B (NF-κB) signalling events in hepatocytes using liver parenchymal cell-specific Nemo knockout (NemoLPC-KO or NemoΔHep) mice that develop steatohepatitis followed …

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