Journal
NATURE COMMUNICATIONS
Volume 8, Issue -, Pages -Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/ncomms13839
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Funding
- Ministry of Science & Technology of China (973 Basic Science Project) [2013CB944902, 2013CB530506]
- Natural Science Foundation of China [81401366, 91429303, 31230025]
- China Postdoctoral Science Foundation [2014M550351, 2015T80661]
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The microbiota control regional immunity using mechanisms such as inducing IL-17A-producing gamma delta T (gamma delta T-17) cells in various tissues. However, little is known regarding hepatic gamma delta T cells that are constantly stimulated by gut commensal microbes. Here we show hepatic gamma delta T cells are liver-resident cells and predominant producers of IL-17A. The microbiota sustain hepatic gamma delta T-17 cell homeostasis, including activation, survival and proliferation. The global commensal quantity affects the number of liver-resident gamma delta T-17 cells; indeed, E. coli alone can generate gamma delta T-17 cells in a dose-dependent manner. Liver-resident gamma delta T-17 cell homeostasis depends on hepatocyte-expressed CD1d, that present lipid antigen, but not Toll-like receptors or IL-1/IL-23 receptor signalling. Supplementing mice in vivo or loading hepatocytes in vitro with exogenous commensal lipid antigens augments the hepatic gamma delta T-17 cell number. Moreover, the microbiota accelerate nonalcoholic fatty liver disease through hepatic gamma delta T-17 cells. Thus, our work describes a unique liver-resident gamma delta T-17 cell subset maintained by gut commensal microbes through CD1d/lipid antigens.
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