| First Author | Li F | Year | 2017 |
| Journal | Nat Commun | Volume | 7 |
| Pages | 13839 | PubMed ID | 28067223 |
| Mgi Jnum | J:243867 | Mgi Id | MGI:5912646 |
| Doi | 10.1038/ncomms13839 | Citation | Li F, et al. (2017) The microbiota maintain homeostasis of liver-resident gammadeltaT-17 cells in a lipid antigen/CD1d-dependent manner. Nat Commun 7:13839 |
| abstractText | The microbiota control regional immunity using mechanisms such as inducing IL-17A-producing gammadelta T (gammadeltaT-17) cells in various tissues. However, little is known regarding hepatic gammadeltaT cells that are constantly stimulated by gut commensal microbes. Here we show hepatic gammadeltaT cells are liver-resident cells and predominant producers of IL-17A. The microbiota sustain hepatic gammadeltaT-17 cell homeostasis, including activation, survival and proliferation. The global commensal quantity affects the number of liver-resident gammadeltaT-17 cells; indeed, E. coli alone can generate gammadeltaT-17 cells in a dose-dependent manner. Liver-resident gammadeltaT-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 gammadeltaT-17 cell number. Moreover, the microbiota accelerate nonalcoholic fatty liver disease through hepatic gammadeltaT-17 cells. Thus, our work describes a unique liver-resident gammadeltaT-17 cell subset maintained by gut commensal microbes through CD1d/lipid antigens. |
