NAFLD causes selective CD4+ T lymphocyte loss and promotes hepatocarcinogenesis View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2016-03

AUTHORS

Chi Ma, Aparna H. Kesarwala, Tobias Eggert, José Medina-Echeverz, David E. Kleiner, Ping Jin, David F. Stroncek, Masaki Terabe, Veena Kapoor, Mei ElGindi, Miaojun Han, Angela M. Thornton, Haibo Zhang, Michèle Egger, Ji Luo, Dean W. Felsher, Daniel W. McVicar, Achim Weber, Mathias Heikenwalder, Tim F. Greten

ABSTRACT

Hepatocellular carcinoma (HCC) is the second most common cause of cancer-related death. Non-alcoholic fatty liver disease (NAFLD) affects a large proportion of the US population and is considered to be a metabolic predisposition to liver cancer. However, the role of adaptive immune responses in NAFLD-promoted HCC is largely unknown. Here we show, in mouse models and human samples, that dysregulation of lipid metabolism in NAFLD causes a selective loss of intrahepatic CD4(+) but not CD8(+) T lymphocytes, leading to accelerated hepatocarcinogenesis. We also demonstrate that CD4(+) T lymphocytes have greater mitochondrial mass than CD8(+) T lymphocytes and generate higher levels of mitochondrially derived reactive oxygen species (ROS). Disruption of mitochondrial function by linoleic acid, a fatty acid accumulated in NAFLD, causes more oxidative damage than other free fatty acids such as palmitic acid, and mediates selective loss of intrahepatic CD4(+) T lymphocytes. In vivo blockade of ROS reversed NAFLD-induced hepatic CD4(+) T lymphocyte decrease and delayed NAFLD-promoted HCC. Our results provide an unexpected link between lipid dysregulation and impaired anti-tumour surveillance. More... »

PAGES

253

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/nature16969

DOI

http://dx.doi.org/10.1038/nature16969

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1025905358

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/26934227


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