A detrimental role of RelB in mature oligodendrocytes during experimental acute encephalomyelitis.

ABSTRACT:

Background

Multiple sclerosis (MS) is an autoimmune demyelinating disease of the central nervous system (CNS). It is firmly established that overactivation of the p65 (RelA) nuclear factor kappa B (NF-κB) transcription factor upregulates expression of inflammatory mediators in both immune and non-immune resident CNS cells and promotes inflammation during MS. In contrast to p65, NF-κB family member RelB regulates immune cell development and can limit inflammation. Although RelB expression is induced during inflammation in the CNS, its role in MS remains unknown.

Methods

To examine the role of RelB in non-immune CNS cells, we generated mice with RelB specifically deleted in astrocytes (RelB^ΔAST), oligodendrocytes (RelB^ΔOLIGO), or neural progenitor-derived

SUBMITTER: Gupta AS 

PROVIDER: S-EPMC6664766 | biostudies-literature | 2019 Jul

REPOSITORIES: biostudies-literature