NDLI: IFN-γ inhibits central nervous system myelination through both STAT1-dependent and STAT1-independent pathways

Content Provider	PubMed Central
Author	Lin, Wensheng Lin, Yifeng
Abstract	Immune cytokine interferon-γ (IFN-γ) plays a crucial role in immune-mediated demyelination diseases such as multiple sclerosis and experimental autoimmune encephalomyelitis (EAE). Our previous studies have shown that enforced expression of IFN-γ in the central nervous system (CNS) inhibits developmental myelination or remyelination in EAE demyelinated lesions. While many of the cellular actions of IFN-γ result from its activation of the signal transducer and activator of transcription 1 (STAT1) pathway, recent studies have shown that STAT1-independent pathways regulate some facets of IFN-γ biology. In this study, we dissected the role of STAT1-dependent and STAT1-independent pathways in IFN-γ-induced hypomyelination using a genetic approach. We found that the induction of the STAT1-dependent, IFN-γ responsive genes in response to this cytokine was abolished in the CNS of STAT1 null mice. Moreover, STAT1 deletion diminished oligodendrocyte loss, the reduction of myelinated axons and inflammatory response in the CNS of transgenic mice that ectopically express IFN-γ in the CNS. Nevertheless, IFN-γ-induced reduction of myelin sheath thickness in the CNS of these mice was not altered by STAT1 deletion. Collectively, these data demonstrated that both STAT1-dependent and STAT1-independent pathways are involved in the detrimental effects of IFN-γ on the myelination process.
Related Links	http://dx.doi.org/10.1002/jnr.22425
Ending Page	2577
Page Count	9
Starting Page	2569
File Format	PDF
ISSN	03604012
e-ISSN	10974547
Journal	Journal of neuroscience research
Issue Number	12
Volume Number	88
Language	English
Publisher Date	2010-01-01
Access Restriction	Open
Subject Keyword	Cellular and Molecular Neuroscience Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Cellular and Molecular Neuroscience

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