Role of nuclear factor κb in multiple sclerosis and experimental autoimmune encephalomyelitis

Yuan Yue, Sarrabeth Stone, Wensheng Lin

Research output: Contribution to journalReview articlepeer-review

14 Scopus citations

Abstract

The transcription factor nuclear factor κB (NF-κB) plays major roles in inflammatory diseases through regulation of inflammation and cell viability. Multiple sclerosis (MS) is a chronic inflammatory demyelinating and neurodegenerative disease of the central nervous system (CNS). It has been shown that NF-κB is activated in multiple cell types in the CNS of MS patients, including T cells, microglia/macrophages, astrocytes, oligodendrocytes, and neurons. Interestingly, data from animal model studies, particularly studies of experimental autoimmune encephalomyelitis, have suggested that NF-κB activation in these individual cell types has distinct effects on the development of MS. In this review, we will cover the current literature on NF-κB and the evidence for its role in the development of MS and its animal model experimental autoimmune encephalomyelitis.

Original languageEnglish (US)
Pages (from-to)1507-1515
Number of pages9
JournalNeural Regeneration Research
Volume13
Issue number9
DOIs
StatePublished - Sep 2018

Bibliographical note

Funding Information:
Funding: This study was supported by grants from the National Institutes of Health (NS094151 and NS105689) and the National Multiple Sclerosis Society (RG5239-A-3) (to WL).

Keywords

  • T cell
  • astrocyte
  • experimental autoimmune encephalomyelitis
  • macrophage
  • microglia
  • multiple sclerosis
  • neuron
  • nuclear-factor ?B
  • oligodendrocyte

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