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Shalapour, Shabnam; Lin, Xue-Jia; Bastian, Ingmar N; Brain, John; Burt, Alastair D; Aksenov, Alexander A; Vrbanac, Alison F; Li, Weihua; Perkins, Andres; Matsutani, Takaji; Zhong, Zhenyu; Dhar, Debanjan; Navas-Molina, Jose A; Xu, Jun; Loomba, Rohit; Downes, Michael; Yu, Ruth T; Evans, Ronald M; Dorrestein, Pieter C; Knight, Rob; Benner, Christopher; Anstee, Quentin M; Karin, Michael
Nature, 11/2017, Letnik: 551, Številka: 7680Journal Article
The role of adaptive immunity in early cancer development is controversial. Here we show that chronic inflammation and fibrosis in humans and mice with non-alcoholic fatty liver disease is accompanied by accumulation of liver-resident immunoglobulin-A-producing (IgA ) cells. These cells also express programmed death ligand 1 (PD-L1) and interleukin-10, and directly suppress liver cytotoxic CD8 T lymphocytes, which prevent emergence of hepatocellular carcinoma and express a limited repertoire of T-cell receptors against tumour-associated antigens. Whereas CD8 T-cell ablation accelerates hepatocellular carcinoma, genetic or pharmacological interference with IgA cell generation attenuates liver carcinogenesis and induces cytotoxic T-lymphocyte-mediated regression of established hepatocellular carcinoma. These findings establish the importance of inflammation-induced suppression of cytotoxic CD8 T-lymphocyte activation as a tumour-promoting mechanism.
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in: SICRIS
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