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pubmed:abstractText |
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.
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