CIRCULATING ADHESION MOLECULES AND INFLAMMATORY MEDIATORS IN DEMYELINATION - A REVIEW

Citation
Hp. Hartung et al., CIRCULATING ADHESION MOLECULES AND INFLAMMATORY MEDIATORS IN DEMYELINATION - A REVIEW, Neurology, 45(6), 1995, pp. 22-32
Citations number
153
Categorie Soggetti
Clinical Neurology
Journal title
ISSN journal
00283878
Volume
45
Issue
6
Year of publication
1995
Supplement
6
Pages
22 - 32
Database
ISI
SICI code
0028-3878(1995)45:6<22:CAMAIM>2.0.ZU;2-K
Abstract
Accumulating evidence shows that adhesion molecules are critically inv olved in inflammatory demyelination in the focusing of systemic immune responses into the target tissue, the nervous system. Adhesion molecu les are upregulated through the action of cytokines. Tumor necrosis fa ctor alpha appears to be of prime importance. Circulating adhesion mol ecules probably reflect acute inflammatory episodes in the central and peripheral nervous system, but may also function to modulate ongoing inflammatory responses. Cytokines released by T(H)1 cells render resid ent and immigrant macrophages, as well as microglia, activated to synt hesize and release increased amounts of inflammatory mediators, such a s oxygen radicals, nitric oxide metabolites, and components of the com plement system. A more detailed understanding of the sequence of immun opathologic events that culminate in myelin damage in the central and peripheral nervous systems has revealed several sites to which more sp ecific and effective immunointervention can be targeted.