Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2019 Aug:80:10-24.
doi: 10.1016/j.bbi.2019.05.029. Epub 2019 May 21.

Astrocytes in multiple sclerosis and experimental autoimmune encephalomyelitis: Star-shaped cells illuminating the darkness of CNS autoimmunity

Affiliations
Review

Astrocytes in multiple sclerosis and experimental autoimmune encephalomyelitis: Star-shaped cells illuminating the darkness of CNS autoimmunity

Wenjing Yi et al. Brain Behav Immun. 2019 Aug.

Abstract

Neuropathology in the human autoimmune disease multiple sclerosis (MS) is considered to be mediated by autoreactive leukocytes, such as T cells, B cells, and macrophages. However, the inflammation and tissue damage in MS and its animal model experimental autoimmune encephalomyelitis (EAE) is also critically regulated by astrocytes, the most abundant cell population in the central nervous system (CNS). Under physiological conditions, astrocytes are integral to the development and function of the CNS, whereas in CNS autoimmunity, astrocytes influence the pathogenesis, progression, and recovery of the diseases. In this review, we summarize recent advances in astrocytic functions in the context of MS and EAE, which are categorized into two opposite aspects, one being detrimental and the other beneficial. Inhibition of the detrimental functions and/or enhancement of the beneficial functions of astrocytes might be favorable for the treatment of MS.

Keywords: Astrocyte; CNS; Demyelination; Experimental autoimmune encephalomyelitis; Multiple sclerosis; Neuroinflammation.

PubMed Disclaimer

Publication types

MeSH terms

LinkOut - more resources