Circulating adhesion molecules and inflammatory mediators in demyelination: a review.

Published

Journal Article (Review)

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.

Full Text

Duke Authors

Cited Authors

  • Hartung, HP; Archelos, JJ; Zielasek, J; Gold, R; Koltzenburg, M; Reiners, KH; Toyka, KV

Published Date

  • June 1995

Published In

Volume / Issue

  • 45 / 6 Suppl 6

Start / End Page

  • S22 - S32

PubMed ID

  • 7783908

Pubmed Central ID

  • 7783908

International Standard Serial Number (ISSN)

  • 0028-3878

Digital Object Identifier (DOI)

  • 10.1212/wnl.45.6_suppl_6.s22

Language

  • eng

Conference Location

  • United States