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NG2 expressed by macrophages and oligodendrocyte precursor cells is dispensable in experimental autoimmune encephalomyelitis

Moransard, Martijn ; Dann, Angela ; Staszewski, Ori ; Fontana, Adriano ; Prinz, Marco ; Suter, Tobias

In: Brain, 2011, vol. 134, no. 5, p. 1315-1330

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    Titre
    • NG2 expressed by macrophages and oligodendrocyte precursor cells is dispensable in experimental autoimmune encephalomyelitis
    Auteur
    • Moransard, Martijn. 1 Clinical Immunology, University Hospital Zurich, Häldeliweg 4, CH-8044 Zürich, Switzerland
    • Dann, Angela. 2 Department of Neuropathology, University of Freiburg, Breisacherstrasse 64, D-79106 Freiburg, Germany
    • Staszewski, Ori. 2 Department of Neuropathology, University of Freiburg, Breisacherstrasse 64, D-79106 Freiburg, Germany
    • Fontana, Adriano. 1 Clinical Immunology, University Hospital Zurich, Häldeliweg 4, CH-8044 Zürich, Switzerland
    • Prinz, Marco. 2 Department of Neuropathology, University of Freiburg, Breisacherstrasse 64, D-79106 Freiburg, Germany
    • Suter, Tobias. 1 Clinical Immunology, University Hospital Zurich, Häldeliweg 4, CH-8044 Zürich, Switzerland
    Type de document
    • Postprint
    Langue
    • Anglais
    Publié dans
    • Brain, 2011, vol. 134, no. 5, p. 1315-1330. Oxford University Press
    Autre version électronique
    Identifiant OAI-PMH
    • oai:doc.rero.ch:292666
    Summary
    Increased expression of the chondroitin proteoglycan NG2 is a prominent feature in central nervous system injury with unknown cellular source and biological relevance. Here, we describe the first detailed analysis of experimental autoimmune encephalomyelitis in NG2 knockout mice and NG2 knockout bone marrow chimeras. We show that both macrophages and oligodendrocyte progenitor cells express and secrete NG2 in response to transforming growth factor-β. A subpopulation of macrophages expresses NG2 within leucocyte infiltrates in the central nervous system, but only oligodendrocyte progenitor cells contribute to NG2 accumulation. Notably, NG2 plays no role in experimental autoimmune encephalomyelitis initiation, progression or recuperation. In concurrence, the immune response is unaltered in NG2-deficient mice as are the extent of central nervous system damage and degree of remyelination