You are seeing this message because your Web browser does not support basic Web standards. Find out more about why this message is appearing and what you can do to make your experience on this site better.


ABOUT ARCHIVES
Advanced Search

Welcome   | My Account | E-mail Alerts | Access Rights | Sign In


  Vol. 60 No. 1, January 2003 TABLE OF CONTENTS
  Archives
  •  Online Features
  Hypothesis
 This Article
 •Full text
 •PDF
 • Reply to article
 •Send to a friend
 • Save in My Folder
 •Save to citation manager
 •Permissions
 Citing Articles
 •Citation map
 •Citing articles on HighWire
 •Citing articles on Web of Science (30)
 •Contact me when this article is cited
 Related Content
 •Similar articles in this journal
 Topic Collections
 •Multiple Sclerosis/ Demyelinating Disease
 •Immunologic Disorders
 •Alert me on articles by topic
 Social Bookmarking
  Add to CiteULike Add to Connotea Add to Del.icio.us Add to Digg Add to Reddit Add to Technorati Add to Twitter What's this?

Are Astrocytes Central Players in the Pathophysiology of Multiple Sclerosis?

Jacques De Keyser, MD; Esther Zeinstra, MD; Elliot Frohman, MD

Arch Neurol. 2003;60:132-136.

An interaction between antimyelin T cells and antigen-presenting glial cells is a crucial step in the cascade of immune events that lead to the inflammatory lesions in multiple sclerosis (MS). One of the most debated and controversial issues is whether microglial cells or astrocytes are the key players in initiating the (auto)immune reactions in the central nervous system in MS. Many investigators consider microglia to be the responsible intrinsic immunoeffector cells. In this review, we speculate that in MS astrocytes may serve as primary (facultative) antigen-presenting cells due to a failure of noradrenergic suppression of class II major histocompatibility complex molecules, which is caused by a loss of {beta}2-adrenergic receptors. If this hypothesis is correct, pharmacologic suppression of the antigen-presenting capacities of astrocytes may be a potential therapy for MS.


From the Departments of Neurology, Academisch Ziekenhuis Groningen, Groningen, the Netherlands (Drs De Keyser and Zeinstra), and University of Texas Southwestern Medical Center at Dallas (Dr Frohman).



Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us   Add to Digg Digg   Add to Reddit Reddit   Add to Technorati Technorati   Add to Twitter Twitter     What's this?

THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES

Effects of fluoxetine on disease activity in relapsing multiple sclerosis: a double-blind, placebo-controlled, exploratory study
Mostert et al.
J. Neurol. Neurosurg. Psychiatry 2008;79:1027-1031.
ABSTRACT | FULL TEXT  

Characterizing the Mechanisms of Progression in Multiple Sclerosis: Evidence and New Hypotheses for Future Directions
Frohman et al.
Arch Neurol 2005;62:1345-1356.
ABSTRACT | FULL TEXT  

DNA microarray analysis of gene expression in human optic nerve head astrocytes in response to hydrostatic pressure
Yang et al.
Physiol. Genomics 2004;17:157-169.
ABSTRACT | FULL TEXT  





HOME | CURRENT ISSUE | PAST ISSUES | TOPIC COLLECTIONS | CME | SUBMIT | SUBSCRIBE | HELP
CONDITIONS OF USE | PRIVACY POLICY | CONTACT US | SITE MAP
 
© 2003 American Medical Association. All Rights Reserved.