AHR activation by tryptophan-Pathogenic hallmark of Th17-mediated inflammation in eosinophilic fasciitis, eosinophilia-myalgia-syndrome and toxic oil syndrome?

Nikolaus Rieber, Bernd H. Belohradsky

Research output: Contribution to journalLetterpeer-review

14 Scopus citations

Abstract

The aryl-hydrocarbon-receptor (AHR) is involved as receptor and transcription factor in dioxin toxicity. Recently, its role in Th17-mediated autoimmunity and autoinflammation has been described, yet a disease-associated AHR ligand is still elusive. l-Tryptophan and its metabolites are assumed to trigger the autoinflammatory disorders eosinophilic fasciitis, eosinophilia-myalgia-syndrome and toxic oil syndrome. Since l-tryptophan and metabolites are well known as AHR ligands we hypothesize that it is their interaction with AHR that induces Th17 cell differentiation and autoinflammation in these disorders. This, for the first time would link disease-causing environmental factors to a well-defined cellular receptor and the subsequent pathogenic pathway.

Original languageEnglish
Pages (from-to)154-155
Number of pages2
JournalImmunology Letters
Volume128
Issue number2
DOIs
StatePublished - Feb 2010
Externally publishedYes

Keywords

  • Aryl-hydrocarbon-receptor (AHR)
  • Autoinflammation
  • Eosinophilia-myalgia-syndrome
  • Eosinophilic fasciitis
  • L-Tryptophan
  • Th17 cells
  • Toxic oil syndrome

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