Interferon β-Mediated Protective Functions of Microglia in Central Nervous System Autoimmunity

  • Stefanie Scheu
    Institute of Medical Microbiology and Hospital Hygiene, University of Düsseldorf, 40225 Düsseldorf, Germany
  • Shafaqat Ali
    Institute of Medical Microbiology and Hospital Hygiene, University of Düsseldorf, 40225 Düsseldorf, Germany
  • Ritu Mann-Nüttel
    Institute of Medical Microbiology and Hospital Hygiene, University of Düsseldorf, 40225 Düsseldorf, Germany
  • Lisa Richter
    Institute of Medical Microbiology and Hospital Hygiene, University of Düsseldorf, 40225 Düsseldorf, Germany
  • Volker Arolt
    Department of Psychiatry and Psychotherapy, University of Münster, 48149 Münster, Germany
  • Udo Dannlowski
    Department of Psychiatry and Psychotherapy, University of Münster, 48149 Münster, Germany
  • Tanja Kuhlmann
    Institute of Neuropathology, University Hospital Münster, 48149, Münster, Germany
  • Luisa Klotz
    Department of Neurology, University of Münster, 48149 Münster, Germany
  • Judith Alferink
    Department of Psychiatry and Psychotherapy, University of Münster, 48149 Münster, Germany

書誌事項

公開日
2019-01-07
権利情報
  • https://creativecommons.org/licenses/by/4.0/
DOI
  • 10.3390/ijms20010190
公開者
MDPI AG

説明

<jats:p>Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system (CNS) leading to demyelination and axonal damage. It often affects young adults and can lead to neurological disability. Interferon β (IFNβ) preparations represent widely used treatment regimens for patients with relapsing-remitting MS (RRMS) with therapeutic efficacy in reducing disease progression and frequency of acute exacerbations. In mice, IFNβ therapy has been shown to ameliorate experimental autoimmune encephalomyelitis (EAE), an animal model of MS while genetic deletion of IFNβ or its receptor augments clinical severity of disease. However, the complex mechanism of action of IFNβ in CNS autoimmunity has not been fully elucidated. Here, we review our current understanding of the origin, phenotype, and function of microglia and CNS immigrating macrophages in the pathogenesis of MS and EAE. In addition, we highlight the emerging roles of microglia as IFNβ-producing cells and vice versa the impact of IFNβ on microglia in CNS autoimmunity. We finally discuss recent progress in unraveling the underlying molecular mechanisms of IFNβ-mediated effects in EAE.</jats:p>

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