Nuclear factor kappa B (NF-κB) in multiple sclerosis pathology

Conor Mc Guire; Marco Prinz; Rudi Beyaert; Geert van Loo

doi:10.1016/j.molmed.2013.08.001

Nuclear factor kappa B (NF-κB) in multiple sclerosis pathology

Trends Mol Med. 2013 Oct;19(10):604-13. doi: 10.1016/j.molmed.2013.08.001. Epub 2013 Sep 2.

Authors

Conor Mc Guire¹, Marco Prinz, Rudi Beyaert, Geert van Loo

Affiliation

¹ Department for Molecular Biomedical Research, Unit of Molecular Signal Transduction in Inflammation, VIB, B-9052 Ghent, Belgium; Department of Biomedical Molecular Biology, Ghent University, B-9052 Ghent, Belgium.

PMID: 24007818
DOI: 10.1016/j.molmed.2013.08.001

Abstract

The nuclear factor kappa B (NF-κB) 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-κB 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-κB 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.

Keywords: NF-κB; Th17; cuprizone; demyelination; experimental autoimmune encephalomyelitis; multiple sclerosis.

Publication types

Research Support, Non-U.S. Gov't
Review

MeSH terms

Animals
Central Nervous System / metabolism
Central Nervous System / pathology
Humans
Inflammation / pathology
Molecular Targeted Therapy
Multiple Sclerosis / immunology
Multiple Sclerosis / metabolism*
Multiple Sclerosis / pathology*
NF-kappa B / metabolism*
Signal Transduction

Substances

NF-kappa B