The microbiota maintain homeostasis of liver-resident γδT-17 cells in a lipid antigen/CD1d-dependent manner

Fenglei Li, Xiaolei Hao, Yongyan Chen, Li Bai, Xiang Gao, Zhexiong Lian, Haiming Wei, Rui Sun and Zhigang Tian ()
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Fenglei Li: Institute of Immunology and the Key Laboratory of Innate Immunity and Chronic Disease (Chinese Academy of Science), School of Life Science and Medical Center, University of Science and Technology of China
Xiaolei Hao: Hefei National Laboratory for Physical Sciences at Microscale
Yongyan Chen: Institute of Immunology and the Key Laboratory of Innate Immunity and Chronic Disease (Chinese Academy of Science), School of Life Science and Medical Center, University of Science and Technology of China
Li Bai: Institute of Immunology and the Key Laboratory of Innate Immunity and Chronic Disease (Chinese Academy of Science), School of Life Science and Medical Center, University of Science and Technology of China
Xiang Gao: Model Animal Research Center, Nanjing University
Zhexiong Lian: Institute of Immunology and the Key Laboratory of Innate Immunity and Chronic Disease (Chinese Academy of Science), School of Life Science and Medical Center, University of Science and Technology of China
Haiming Wei: Institute of Immunology and the Key Laboratory of Innate Immunity and Chronic Disease (Chinese Academy of Science), School of Life Science and Medical Center, University of Science and Technology of China
Rui Sun: Institute of Immunology and the Key Laboratory of Innate Immunity and Chronic Disease (Chinese Academy of Science), School of Life Science and Medical Center, University of Science and Technology of China
Zhigang Tian: Institute of Immunology and the Key Laboratory of Innate Immunity and Chronic Disease (Chinese Academy of Science), School of Life Science and Medical Center, University of Science and Technology of China

Nature Communications, 2017, vol. 8, issue 1, 1-15

Abstract: Abstract The microbiota control regional immunity using mechanisms such as inducing IL-17A-producing γδ T (γδT-17) cells in various tissues. However, little is known regarding hepatic γδT cells that are constantly stimulated by gut commensal microbes. Here we show hepatic γδT cells are liver-resident cells and predominant producers of IL-17A. The microbiota sustain hepatic γδT-17 cell homeostasis, including activation, survival and proliferation. The global commensal quantity affects the number of liver-resident γδT-17 cells; indeed, E. coli alone can generate γδT-17 cells in a dose-dependent manner. Liver-resident γδT-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 γδT-17 cell number. Moreover, the microbiota accelerate nonalcoholic fatty liver disease through hepatic γδT-17 cells. Thus, our work describes a unique liver-resident γδT-17 cell subset maintained by gut commensal microbes through CD1d/lipid antigens.

Date: 2017
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DOI: 10.1038/ncomms13839

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