Abstract:
: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.
journal_name
Naturejournal_title
Natureauthors
Shalapour S,Lin XJ,Bastian IN,Brain J,Burt AD,Aksenov AA,Vrbanac AF,Li W,Perkins A,Matsutani T,Zhong Z,Dhar D,Navas-Molina JA,Xu J,Loomba R,Downes M,Yu RT,Evans RM,Dorrestein PC,Knight R,Benner C,Anstee QM,Kardoi
10.1038/nature24302subject
Has Abstractpub_date
2017-11-16 00:00:00pages
340-345issue
7680eissn
0028-0836issn
1476-4687pii
nature24302journal_volume
551pub_type
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