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Tumor necrosis factor alpha (TNF-α), anti-TNF-α and demyelination revisited: an ongoing story.

Abstract
Tumor necrosis factor alpha (TNF-α) is a cytokine with pleiotropic actions that can be present both as a transmembrane protein and soluble cytokine (sTNF). Both ligands interact with two different receptors, TNFR1 and TNFR2, which mediate their biological effects. TNF-α is involved in the pathogenesis of multiple sclerosis (MS), however, administration of anti-TNF-α agents to MS patients has been associated with increased disease activity. Insomuch as TNFR1 mediates demyelination and TNFR2 remyelination, it could be hypothesized that anti-TNF-α agents which selectively inhibit sTNF or signals from TNFR1 could be effective in treating MS.
AuthorsAna Caminero, Manuel Comabella, Xavier Montalban
JournalJournal of neuroimmunology (J Neuroimmunol) Vol. 234 Issue 1-2 Pg. 1-6 (May 2011) ISSN: 1872-8421 [Electronic] Netherlands
PMID21474190 (Publication Type: Journal Article, Review)
CopyrightCopyright © 2011 Elsevier B.V. All rights reserved.
Chemical References
  • Antibodies
  • Receptors, Tumor Necrosis Factor, Type I
  • Receptors, Tumor Necrosis Factor, Type II
  • Tumor Necrosis Factor-alpha
Topics
  • Animals
  • Antibodies (therapeutic use)
  • Disease Models, Animal
  • Humans
  • Models, Biological
  • Multiple Sclerosis (therapy)
  • Receptors, Tumor Necrosis Factor, Type I (metabolism)
  • Receptors, Tumor Necrosis Factor, Type II (metabolism)
  • Tumor Necrosis Factor-alpha (antagonists & inhibitors, immunology, metabolism)

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