Nur77 serves as a molecular brake of the metabolic switch during T cell activation to restrict autoimmunity

DOI Web Site Web Site 1 Citations
  • Marie Liebmann
    Department of Neurology with Institute of Translational Neurology, University Hospital Muenster, 48149 Muenster, Germany;
  • Stephanie Hucke
    Department of Neurology with Institute of Translational Neurology, University Hospital Muenster, 48149 Muenster, Germany;
  • Kathrin Koch
    Department of Neurology with Institute of Translational Neurology, University Hospital Muenster, 48149 Muenster, Germany;
  • Melanie Eschborn
    Department of Neurology with Institute of Translational Neurology, University Hospital Muenster, 48149 Muenster, Germany;
  • Julia Ghelman
    Institute of Neuropathology, University Hospital Muenster, 48149 Muenster, Germany;
  • Achmet I. Chasan
    Institute of Immunology, University of Muenster, 48149 Muenster, Germany;
  • Shirin Glander
    Department of Genetic Epidemiology, Institute of Human Genetics, University of Muenster, 48149 Muenster, Germany;
  • Martin Schädlich
    Department of Genetic Epidemiology, Institute of Human Genetics, University of Muenster, 48149 Muenster, Germany;
  • Meike Kuhlencord
    Institute of Immunology, University of Muenster, 48149 Muenster, Germany;
  • Niklas M. Daber
    Institute of Immunology, University of Muenster, 48149 Muenster, Germany;
  • Maria Eveslage
    Institute of Biostatistics and Clinical Research, University of Muenster, 48149 Muenster, Germany;
  • Marc Beyer
    Department of Genomics and Immunoregulation, Life and Medical Sciences Institute, University of Bonn, 53115 Bonn, Germany;
  • Michael Dietrich
    Department of Neurology, University of Düsseldorf, 40225 Düsseldorf, Germany;
  • Philipp Albrecht
    Department of Neurology, University of Düsseldorf, 40225 Düsseldorf, Germany;
  • Monika Stoll
    Department of Genetic Epidemiology, Institute of Human Genetics, University of Muenster, 48149 Muenster, Germany;
  • Karin B. Busch
    Institute for Molecular Cell Biology, University of Muenster, 48149 Muenster, Germany
  • Heinz Wiendl
    Department of Neurology with Institute of Translational Neurology, University Hospital Muenster, 48149 Muenster, Germany;
  • Johannes Roth
    Institute of Immunology, University of Muenster, 48149 Muenster, Germany;
  • Tanja Kuhlmann
    Institute of Neuropathology, University Hospital Muenster, 48149 Muenster, Germany;
  • Luisa Klotz
    Department of Neurology with Institute of Translational Neurology, University Hospital Muenster, 48149 Muenster, Germany;

Description

<jats:title>Significance</jats:title> <jats:p>The role of metabolic processes during T cell activation has been increasingly acknowledged, and recent data suggest an impact of T cell immunometabolism on T cell function and T cell-mediated autoimmunity. The factors regulating metabolic function in T cells are not clear, however. We identify the nuclear receptor Nur77 as central regulator of T cell immunometabolism, controlling oxidative phosphorylation and aerobic glycolysis during T cell activation. Functionally, Nur77 restricts murine and human T cell activation and proliferation and limits inflammation in autoimmune conditions in animal models of CNS autoimmunity, contact dermatitis, and arthritis. These findings identify Nur77 as a central regulator of T cell immunometabolism that restricts T cell-mediated autoimmunity, which might open up new avenues for a more tailored therapeutic approach.</jats:p>

Journal

Citations (1)*help

See more

Report a problem

Back to top