Neurology
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

This Article
Right arrow Correspondence:
Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when Correspondence are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Hartung, H. P.
Right arrow Articles by Toyka, K. V.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Hartung, H. P.
Right arrow Articles by Toyka, K. V.

Neurology, Vol 45, Issue 6 S22-S32, Copyright © 1995 by American Academy of Neurology

VIEWS & REVIEWS

Circulating adhesion molecules and inflammatory mediators in demyelination: a review

HP Hartung, JJ Archelos, J Zielasek, R Gold, M Koltzenburg, KH Reiners and KV Toyka
Department of Neurology, Julius-Maximilians-Universitat, Wurzburg, Germany.

Accumulating evidence shows that adhesion molecules are critically involved in inflammatory demyelination in the focusing of systemic immune responses into the target tissue, the nervous system. Adhesion molecules are upregulated through the action of cytokines. Tumor necrosis factor alpha appears to be of prime importance. Circulating adhesion molecules probably reflect acute inflammatory episodes in the central and peripheral nervous system, but may also function to modulate ongoing inflammatory responses. Cytokines released by TH1 cells render resident and immigrant macrophages, as well as microglia, activated to synthesize and release increased amounts of inflammatory mediators, such as oxygen radicals, nitric oxide metabolites, and components of the complement system. A more detailed understanding of the sequence of immunopathologic events that culminate in myelin damage in the central and peripheral nervous systems has revealed several sites to which more specific and effective immunointervention can be targeted.


This article has been cited by other articles:


Home page
 Arch NeurolHome page
H. C. Lehmann, H.-P. Hartung, G. R. Hetzel, O. Stuve, and B. C. Kieseier
Plasma exchange in neuroimmunological disorders: part 1: rationale and treatment of inflammatory central nervous system disorders.
Arch Neurol, July 1, 2006; 63(7): 930 - 935.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 1995 by AAN Enterprises, Inc.