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

J Neuroimmunol. 2011 May;234(1-2):1-6. doi: 10.1016/j.jneuroim.2011.03.004. Epub 2011 Apr 7.


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.

Publication types

  • Review

MeSH terms

  • 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
  • Tumor Necrosis Factor-alpha* / immunology
  • Tumor Necrosis Factor-alpha* / metabolism


  • Antibodies
  • Receptors, Tumor Necrosis Factor, Type I
  • Receptors, Tumor Necrosis Factor, Type II
  • Tumor Necrosis Factor-alpha