Title: Oncostatin M protects against demyelination by inducing a protective microglial phenotype
Authors: Janssens, Kris ×
Maheshwari, Anurag
Van Den Haute, Chris
Baekelandt, Veerle
Stinissen, Piet
Hendriks, Jerome JA
Slaets, Helena
Hellings, Niels #
Issue Date: 2015
Publisher: Wiley-Liss, Inc.
Series Title: GLIA vol:63 issue:10 pages:1729-1737
Abstract: Multiple sclerosis (MS) is a chronic disabling disease of the central nervous system (CNS), in which destruction of myelin sheaths leads to disturbed axonal conduction. Available MS therapies modulate the immune response, but are unable to prevent neurological decline. Therefore, great efforts are made to develop therapies that limit demyelination and axonal degeneration. Oncostatin M (OSM), a member of the interleukin (IL)-6 cytokine family, is produced in demyelinating lesions of MS patients and stimulates neuronal survival. In this study, we reveal that the OSM receptor (OSMR) was robustly upregulated on microglia/macrophages and astrocytes in the cuprizone-induced demyelination model. While OSMR deficiency led to aggravated demyelination, CNS-targeted OSM treatment largely prevented demyelination. OSM treatment increased IL-4 expression and induced polarization of myeloid cells towards an anti-inflammatory M2 phenotype in vivo. This study reveals a previously uncharacterized and protective role for OSM during demyelination, and indicates that OSM is a promising therapeutic candidate to limit CNS damage in demyelinating diseases including MS. GLIA 2015;63:1729-1737.
ISSN: 0894-1491
Publication status: published
KU Leuven publication type: IT
Appears in Collections:Research Group for Neurobiology and Gene Therapy
× corresponding author
# (joint) last author

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