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. 2014 Oct 13;26(4):549-64.
doi: 10.1016/j.ccell.2014.09.003.

Metabolic activation of intrahepatic CD8+ T cells and NKT cells causes nonalcoholic steatohepatitis and liver cancer via cross-talk with hepatocytes

Monika Julia Wolf  1 , Arlind Adili  2 , Kira Piotrowitz  3 , Zeinab Abdullah  4 , Yannick Boege  1 , Kerstin Stemmer  5 , Marc Ringelhan  6 , Nicole Simonavicius  2 , Michèle Egger  1 , Dirk Wohlleber  7 , Anna Lorentzen  2 , Claudia Einer  8 , Sabine Schulz  8 , Thomas Clavel  9 , Ulrike Protzer  2 , Christoph Thiele  3 , Hans Zischka  8 , Holger Moch  1 , Matthias Tschöp  5 , Alexei V Tumanov  10 , Dirk Haller  11 , Kristian Unger  12 , Michael Karin  13 , Manfred Kopf  14 , Percy Knolle  15 , Achim Weber  16 , Mathias Heikenwalder  17
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"VSports" Metabolic activation of intrahepatic CD8+ T cells and NKT cells causes nonalcoholic steatohepatitis and liver cancer via cross-talk with hepatocytes

Monika Julia Wolf et al. Cancer Cell. .
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Abstract

Hepatocellular carcinoma (HCC), the fastest rising cancer in the United States and increasing in Europe, often occurs with nonalcoholic steatohepatitis (NASH). Mechanisms underlying NASH and NASH-induced HCC are largely unknown. We developed a mouse model recapitulating key features of human metabolic syndrome, NASH, and HCC by long-term feeding of a choline-deficient high-fat diet. This induced activated intrahepatic CD8(+) T cells, NKT cells, and inflammatory cytokines, similar to NASH patients. CD8(+) T cells and NKT cells but not myeloid cells promote NASH and HCC through interactions with hepatocytes VSports手机版. NKT cells primarily cause steatosis via secreted LIGHT, while CD8(+) and NKT cells cooperatively induce liver damage. Hepatocellular LTβR and canonical NF-κB signaling facilitate NASH-to-HCC transition, demonstrating that distinct molecular mechanisms determine NASH and HCC development. .

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