The aryl hydrocarbon receptor links TH17-cell-mediated autoimmunity to environmental toxins
Marc Veldhoen,
Keiji Hirota,
Astrid M. Westendorf,
Jan Buer,
Laure Dumoutier,
Jean-Christophe Renauld and
Brigitta Stockinger ()
Additional contact information
Marc Veldhoen: MRC National Institute for Medical Research, The Ridgeway, Mill Hill, London NW71AA, UK
Keiji Hirota: MRC National Institute for Medical Research, The Ridgeway, Mill Hill, London NW71AA, UK
Astrid M. Westendorf: Institute for Medical Microbiology, University Hospital Essen, D-45122, Germany
Jan Buer: Institute for Medical Microbiology, University Hospital Essen, D-45122, Germany
Laure Dumoutier: Ludwig Institute for Cancer Research, Brussels branch, and Experimental Medicine Unit, Universite Catholique de Louvain
Jean-Christophe Renauld: Ludwig Institute for Cancer Research, Brussels branch, and Experimental Medicine Unit, Universite Catholique de Louvain
Brigitta Stockinger: MRC National Institute for Medical Research, The Ridgeway, Mill Hill, London NW71AA, UK
Nature, 2008, vol. 453, issue 7191, 106-109
Abstract:
Toxins and autoimmunity The aryl hydrocarbon receptor (AHR) is a transcription factor best known for mediating the toxicity of aromatic hydrocarbons such as dioxin: its activation leads to the production of detoxification enzymes. AHR has been intensely studied in relation to toxicology and cancer research, but no mechanistic connection to the immune system was known. Now two groups report a role for AHR in maintaining the balance between two T-lymphocyte populations — the Treg and TH17 cells — that are part of the immune regulation system dealing with tolerance of self-antigens and pathogen clearance. Both groups also show that AHR affects the severity of experimental autoimmune encephalitis, a mouse model of multiple sclerosis. This work raises the possibility that stimulation of AHR by environmental factors could be involved in the development of autoimmune disease, and point to AHR as a possible drug target for immunomodulation.
Date: 2008
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DOI: 10.1038/nature06881
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