Journal
TRENDS IN MOLECULAR MEDICINE
Volume 19, Issue 10, Pages 604-613Publisher
ELSEVIER SCI LTD
DOI: 10.1016/j.molmed.2013.08.001
Keywords
multiple sclerosis; experimental autoimmune encephalomyelitis; cuprizone; NF-kappa B; demyelination; Th17
Funding
- Fonds voor Wetenschappelijk Onderzoek-Vlaanderen (FWO)
- FWO Odysseus Grant
- Geneeskundige Stichting Koningin Elisabeth (GSKE)
- Charcot Foundation
- Interuniversity Attraction Poles program [IAP7/32]
- FWO
- Belgian Foundation against Cancer
- Strategic Basis Research program of the IWT
- Group-ID MRP, GOA
- Hercules initiatives of Ghent University
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The nuclear factor kappa B (NF-kappa B) signaling cascade plays a critical role in the regulation of immune and inflammatory responses and has been implicated in the pathogenesis of autoimmune demyelinating diseases such as multiple sclerosis (MS) and experimental autoimmune encephalomyelitis (EAE), the main animal model of MS. NF-kappa B is essential for peripheral immune cell activation and the induction of pathology, but also plays crucial roles in resident cells of the central nervous system (CNS) during disease development. Here we review recent evidence clarifying the role of NF-kappa B in the different cell compartments contributing to MS pathology and its implications for the development of therapeutic strategies for the treatment of MS and other demyelinating pathologies of the CNS.
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