Tumor necrosis factor-α in Guillain-Barré syndrome, friend or foe?

Expert Opin Ther Targets. 2017 Jan;21(1):103-112. doi: 10.1080/14728222.2017.1258402. Epub 2016 Nov 18.

Abstract

Guillain-Barré syndrome (GBS) is an immune-mediated disorder in the peripheral nervous system (PNS), and experimental autoimmune neuritis (EAN) serves as an animal model of GBS. TNF-α plays an important role in the pathogenesis of GBS and is a potential therapeutic target of GBS. Areas covered: 'TNF-α' and 'Guillain-Barré syndrome' were the keywords used to search for related publications on Pubmed. By binding to different TNF receptors, TNF-α bears distinct immune properties. TNF-α gene polymorphisms are associated with the features of GBS. The major role of TNF-α in GBS/EAN is to aggravate inflammation; however, data from several studies indicated a protective role of TNF-α. Multiple lines of evidence point to TNF-α as a potential therapeutic target for GBS. However, such clinical trials are scarce in that GBS per se is a probable side effect of anti-TNF-α treatment. Expert opinion: TNF-α plays a dual role in GBS and EAN, and is a potential therapeutic target on GBS/EAN.

Keywords: Experimental autoimmune neuritis; Guillain-Barré syndrome; TNF-α; therapeutic target.

Publication types

  • Review

MeSH terms

  • Animals
  • Disease Models, Animal
  • Guillain-Barre Syndrome / drug therapy*
  • Guillain-Barre Syndrome / physiopathology
  • Humans
  • Inflammation / pathology
  • Molecular Targeted Therapy*
  • Neuritis, Autoimmune, Experimental / drug therapy
  • Neuritis, Autoimmune, Experimental / physiopathology
  • Polymorphism, Genetic
  • Tumor Necrosis Factor-alpha / genetics
  • Tumor Necrosis Factor-alpha / metabolism*

Substances

  • Tumor Necrosis Factor-alpha