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Control of Treg and TH17 cell differentiation by the aryl hydrocarbon receptor

Author

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  • Francisco J. Quintana

    (Center for Neurologic Diseases, Brigham and Women’s Hospital, Harvard Medical School, 77 Avenue Louis Pasteur, Boston, Massachusetts 02115, USA)

  • Alexandre S. Basso

    (Center for Neurologic Diseases, Brigham and Women’s Hospital, Harvard Medical School, 77 Avenue Louis Pasteur, Boston, Massachusetts 02115, USA)

  • Antonio H. Iglesias

    (Center for Neurologic Diseases, Brigham and Women’s Hospital, Harvard Medical School, 77 Avenue Louis Pasteur, Boston, Massachusetts 02115, USA)

  • Thomas Korn

    (Center for Neurologic Diseases, Brigham and Women’s Hospital, Harvard Medical School, 77 Avenue Louis Pasteur, Boston, Massachusetts 02115, USA)

  • Mauricio F. Farez

    (Center for Neurologic Diseases, Brigham and Women’s Hospital, Harvard Medical School, 77 Avenue Louis Pasteur, Boston, Massachusetts 02115, USA)

  • Estelle Bettelli

    (Center for Neurologic Diseases, Brigham and Women’s Hospital, Harvard Medical School, 77 Avenue Louis Pasteur, Boston, Massachusetts 02115, USA)

  • Mario Caccamo

    (EMBL Outstation – Hinxton, European Bioinformatics Institute, Wellcome Trust Genome Campus, Hinxton, Cambridge CB10 1SD, UK)

  • Mohamed Oukka

    (Center for Neurologic Diseases, Brigham and Women’s Hospital, Harvard Medical School, 65 Landsdowne Street, Cambridge, Massachusetts 02139, USA)

  • Howard L. Weiner

    (Center for Neurologic Diseases, Brigham and Women’s Hospital, Harvard Medical School, 77 Avenue Louis Pasteur, Boston, Massachusetts 02115, USA)

Abstract

Regulatory T cells (Treg) expressing the transcription factor Foxp3 control the autoreactive components of the immune system. The development of Treg cells is reciprocally related to that of pro-inflammatory T cells producing interleukin-17 (TH17). Although Treg cell dysfunction and/or TH17 cell dysregulation are thought to contribute to the development of autoimmune disorders, little is known about the physiological pathways that control the generation of these cell lineages. Here we report the identification of the ligand-activated transcription factor aryl hydrocarbon receptor (AHR) as a regulator of Treg and TH17 cell differentiation in mice. AHR activation by its ligand 2,3,7,8-tetrachlorodibenzo-p-dioxin induced functional Treg cells that suppressed experimental autoimmune encephalomyelitis. On the other hand, AHR activation by 6-formylindolo[3,2-b]carbazole interfered with Treg cell development, boosted TH17 cell differentiation and increased the severity of experimental autoimmune encephalomyelitis in mice. Thus, AHR regulates both Treg and TH17 cell differentiation in a ligand-specific fashion, constituting a unique target for therapeutic immunomodulation.

Suggested Citation

  • Francisco J. Quintana & Alexandre S. Basso & Antonio H. Iglesias & Thomas Korn & Mauricio F. Farez & Estelle Bettelli & Mario Caccamo & Mohamed Oukka & Howard L. Weiner, 2008. "Control of Treg and TH17 cell differentiation by the aryl hydrocarbon receptor," Nature, Nature, vol. 453(7191), pages 65-71, May.
    • Handle: RePEc:nat:nature:v:453:y:2008:i:7191:d:10.1038_nature06880
    DOI: 10.1038/nature06880
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    Cited by:

    1. Nguyen T. Van & Karen Zhang & Rachel M. Wigmore & Anne I. Kennedy & Carolina R. DaSilva & Jialing Huang & Manju Ambelil & Jose H. Villagomez & Gerald J. O’Connor & Randy S. Longman & Miao Cao & Adam E, 2023. "Dietary L-Tryptophan consumption determines the number of colonic regulatory T cells and susceptibility to colitis via GPR15," Nature Communications, Nature, vol. 14(1), pages 1-15, December.
    2. Han Zhang & Rahul Kalla & Jie Chen & Jianhui Zhao & Xuan Zhou & Alex Adams & Alexandra Noble & Nicholas T. Ventham & Judith Wellens & Gwo-Tzer Ho & Malcolm G. Dunlop & Jan Krzysztof Nowak & Yuan Ding , 2024. "Altered DNA methylation within DNMT3A, AHRR, LTA/TNF loci mediates the effect of smoking on inflammatory bowel disease," Nature Communications, Nature, vol. 15(1), pages 1-14, December.

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