Veldhoen, M.; Hirota, K.; Stockinger, B.; Westendorf, Astrid; Buer, Jan; Renauld, J.C.; Dumoutier, L::
The aryl hydrocarbon receptor links TH17-cell-mediated autoimmunity to environmental toxins
In: Nature, Vol. 453 (2008), No. 7191, pp. 106 - 109
2008article/chapter in journalOA Green
MedicineScientific institutes » Center of Medical Biotechnology (ZMB) Faculty of Medicine » Essen University Hospital » Institute of Medical Microbiology
Title in English:
The aryl hydrocarbon receptor links TH17-cell-mediated autoimmunity to environmental toxins
Author:
Veldhoen, M.;Hirota, K.;Stockinger, B.;Westendorf, AstridUDE
GND
1209772027
LSF ID
49459
ORCID
0000-0002-2121-2892ORCID iD
Other
connected with university
;
Buer, JanUDE
GND
133594114
LSF ID
49456
ORCID
0000-0002-7602-1698ORCID iD
Other
connected with university
;
Renauld, J.C.;Dumoutier, L:
Year of publication:
2008
Open Access?:
OA Green
Web of Science ID
PubMed ID
Scopus ID
Language of text:
English

Abstract in English:

The aryl hydrocarbon receptor (AHR) is a ligand-dependent transcription factor best known for mediating the toxicity of dioxin. Environmental factors are believed to contribute to the increased prevalence of autoimmune diseases, many of which are due to the activity of TH17 T cells, a new helper T-cell subset characterized by the production of the cytokine IL-17. Here we show that in the CD4+ T-cell lineage of mice AHR expression is restricted to the TH17 cell subset and its ligation results in the production of the TH17 cytokine interleukin (IL)-22. AHR is also expressed in human TH17 cells. Activation of AHR by a high-affinity ligand during TH17 cell development markedly increases the proportion of TH17 T cells and their production of cytokines. CD4+ T cells from AHR-deficient mice can develop TH17 cell responses, but when confronted with AHR ligand fail to produce IL-22 and do not show enhanced TH17 cell development. AHR activation during induction of experimental autoimmune encephalomyelitis causes accelerated onset and increased pathology in wild-type mice, but not AHR-deficient mice. AHR ligands may therefore represent co-factors in the development of autoimmune diseases.