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

Neural Regen Res. 2018 Sep;13(9):1507-1515. doi: 10.4103/1673-5374.237109.

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.

Keywords: T cell; astrocyte; experimental autoimmune encephalomyelitis; macrophage; microglia; multiple sclerosis; neuron; nuclear-factor κB; oligodendrocyte.

Publication types

  • Review