Nur77 serves as a molecular brake of the metabolic switch during T cell activation to restrict autoimmunity
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- Marie Liebmann
- Department of Neurology with Institute of Translational Neurology, University Hospital Muenster, 48149 Muenster, Germany;
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- Stephanie Hucke
- Department of Neurology with Institute of Translational Neurology, University Hospital Muenster, 48149 Muenster, Germany;
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- Kathrin Koch
- Department of Neurology with Institute of Translational Neurology, University Hospital Muenster, 48149 Muenster, Germany;
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- Melanie Eschborn
- Department of Neurology with Institute of Translational Neurology, University Hospital Muenster, 48149 Muenster, Germany;
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- Julia Ghelman
- Institute of Neuropathology, University Hospital Muenster, 48149 Muenster, Germany;
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- Achmet I. Chasan
- Institute of Immunology, University of Muenster, 48149 Muenster, Germany;
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- Shirin Glander
- Department of Genetic Epidemiology, Institute of Human Genetics, University of Muenster, 48149 Muenster, Germany;
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- Martin Schädlich
- Department of Genetic Epidemiology, Institute of Human Genetics, University of Muenster, 48149 Muenster, Germany;
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- Meike Kuhlencord
- Institute of Immunology, University of Muenster, 48149 Muenster, Germany;
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- Niklas M. Daber
- Institute of Immunology, University of Muenster, 48149 Muenster, Germany;
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- Maria Eveslage
- Institute of Biostatistics and Clinical Research, University of Muenster, 48149 Muenster, Germany;
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- Marc Beyer
- Department of Genomics and Immunoregulation, Life and Medical Sciences Institute, University of Bonn, 53115 Bonn, Germany;
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- Michael Dietrich
- Department of Neurology, University of Düsseldorf, 40225 Düsseldorf, Germany;
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- Philipp Albrecht
- Department of Neurology, University of Düsseldorf, 40225 Düsseldorf, Germany;
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- Monika Stoll
- Department of Genetic Epidemiology, Institute of Human Genetics, University of Muenster, 48149 Muenster, Germany;
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- Karin B. Busch
- Institute for Molecular Cell Biology, University of Muenster, 48149 Muenster, Germany
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- Heinz Wiendl
- Department of Neurology with Institute of Translational Neurology, University Hospital Muenster, 48149 Muenster, Germany;
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- Johannes Roth
- Institute of Immunology, University of Muenster, 48149 Muenster, Germany;
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- Tanja Kuhlmann
- Institute of Neuropathology, University Hospital Muenster, 48149 Muenster, Germany;
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- Luisa Klotz
- Department of Neurology with Institute of Translational Neurology, University Hospital Muenster, 48149 Muenster, Germany;
説明
<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>
収録刊行物
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- Proceedings of the National Academy of Sciences
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Proceedings of the National Academy of Sciences 115 (34), E8017-, 2018-08-02
Proceedings of the National Academy of Sciences