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Gewählte Publikation:

Hartung, HP; Archelos, JJ; Zielasek, J; Gold, R; Koltzenburg, M; Reiners, KH; Toyka, KV.
Circulating adhesion molecules and inflammatory mediators in demyelination: a review.
Neurology. 1995; 45(6 Suppl 6):S22-S32 Doi: 10.1212/WNL.45.6_Suppl_6.S22
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Co-Autor*innen der Med Uni Graz
Archelos-Garcia Juan-Jose
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Abstract:
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.
Find related publications in this database (using NLM MeSH Indexing)
Cell Adhesion Molecules - metabolism
Complement System Proteins - metabolism
Cytokines - metabolism
Demyelinating Diseases - immunology
Encephalomyelitis, Autoimmune, Experimental - immunology
Humans - immunology
Inflammation Mediators - metabolism
Multiple Sclerosis - immunology
Polyradiculoneuropathy - immunology
T-Lymphocytes - metabolism

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