Aryl hydrocarbon receptor regulates Stat1 activation and participates in the development of Th17 cells

Akihiro Kimura, Tetsuji Naka, Keiko Nohara, Yoshiaki Fujii-Kuriyama, Tadamitsu Kishimoto

Research output: Contribution to journalArticle

343 Citations (Scopus)

Abstract

IL-17-producing T helper cells (Th17) have been recently identified as a previously undescribed subset of helper T cells. Here, we demonstrate that aryl hydrocarbon receptor (Ahr) has an important regulatory function in the commitment of Th17 cells. Ahr was robustly induced under Th17-polarizing conditions. Ahr-deficient naïve T cells showed a considerable loss in the ability to differentiate into Th17 cells when induced by TGF-β plus IL-6. We were able to demonstrate that Ahr interacts with Stat1 and Stat5, which negatively regulate Th17 development. Whereas Stat1 activation returned to its basal level in Ahr wild type naïve T cells 24 h after stimulation with TGF-β plus IL-6, Stat1 remained activated in Ahr-deficient naïve T cells after stimulation. These results indicate that Ahr participates in Th17 cell differentiation through regulating Stat1 activation, a finding that constitutes additional mechanisms in the modulation of Th17 cell development.

Original languageEnglish
Pages (from-to)9721-9726
Number of pages6
JournalProceedings of the National Academy of Sciences of the United States of America
Volume105
Issue number28
DOIs
Publication statusPublished - 2008 Jul 15

Keywords

  • Dioxin receptor
  • IL-17
  • IL-6
  • ROR
  • Regulatory T cells

ASJC Scopus subject areas

  • General

Fingerprint Dive into the research topics of 'Aryl hydrocarbon receptor regulates Stat1 activation and participates in the development of Th17 cells'. Together they form a unique fingerprint.

  • Cite this