Acetate Promotes T Cell Effector Function during Glucose Restriction
Jing QiuMax Planck Institute of Immunobiology and Epigenetics, Freiburg 79108, GermanyMatteo VillaMax Planck Institute of Immunobiology and Epigenetics, Freiburg 79108, GermanyDavid E. SaninMax Planck Institute of Immunobiology and Epigenetics, Freiburg 79108, GermanyMichael D. BuckMax Planck Institute of Immunobiology and Epigenetics, Freiburg 79108, GermanyDavid O’SullivanMax Planck Institute of Immunobiology and Epigenetics, Freiburg 79108, GermanyReagan W. ChingMax Planck Institute of Immunobiology and Epigenetics, Freiburg 79108, GermanyMai MatsushitaMax Planck Institute of Immunobiology and Epigenetics, Freiburg 79108, GermanyKatarzyna M. GrzesMax Planck Institute of Immunobiology and Epigenetics, Freiburg 79108, GermanyFrances WinklerFaculty of Biology, University of Freiburg, 79104 Freiburg, GermanyChih‐Hao ChangThe Jackson Laboratory, Bar Harbor, ME 04609, USAJonathan D. CurtisMax Planck Institute of Immunobiology and Epigenetics, Freiburg 79108, GermanyRyan KyleMax Planck Institute of Immunobiology and Epigenetics, Freiburg 79108, GermanyNikki van Teijlingen BakkerMax Planck Institute of Immunobiology and Epigenetics, Freiburg 79108, GermanyMauro CorradoMax Planck Institute of Immunobiology and Epigenetics, Freiburg 79108, GermanyFabian HaesslerMax Planck Institute of Immunobiology and Epigenetics, Freiburg 79108, GermanyFrancesca AlfeiSchool of Life Science, Technical University of Munich, 80333 Munich, GermanyJoy Edwards-HicksMax Planck Institute of Immunobiology and Epigenetics, Freiburg 79108, GermanyLeonard B. MaggiICCE Institute and Department of Medicine, Division of Molecular Oncology, Siteman Cancer Center, Washington University School of Medicine, St. Louis, MO 63110, USADietmar ZehnSchool of Life Science, Technical University of Munich, 80333 Munich, GermanyTakeshi EgawaDepartment of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110, USABertram BengschBIOSS Center for Biological Signaling Studies, University of Freiburg, 79104 Freiburg, GermanyRamon I. Klein GeltinkMax Planck Institute of Immunobiology and Epigenetics, Freiburg 79108, GermanyThomas JenuweinMax Planck Institute of Immunobiology and Epigenetics, Freiburg 79108, GermanyEdward J. PearceMax Planck Institute of Immunobiology and Epigenetics, Freiburg 79108, Germany. Electronic address: [email protected]Erika L. PearceMax Planck Institute of Immunobiology and Epigenetics, Freiburg 79108, Germany. Electronic address: [email protected]
2019en
ABI
Annotatsiya
T cells. Mechanistically, acetate promotes histone acetylation and chromatin accessibility and enhances IFN-γ gene transcription and cytokine production in an acetyl-CoA synthetase (ACSS)-dependent manner. Ex vivo acetate treatment increases IFN-γ production by exhausted T cells, whereas reducing ACSS expression in T cells impairs IFN-γ production by tumor-infiltrating lymphocytes and tumor clearance. Thus, hyporesponsive T cells can be epigenetically remodeled and reactivated by acetate, suggesting that pathways regulating the use of substrates alternative to glucose could be therapeutically targeted to promote T cell function during cancer.
Hali tarjima qilinmagan
Identifikatorlar
Iqtiboslar va manbalar
2 ta iqtibos0 ta foydalanilgan manba