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

研究成果: Article査読

392 被引用数 (Scopus)

抄録

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.

本文言語English
ページ(範囲)9721-9726
ページ数6
ジャーナルProceedings of the National Academy of Sciences of the United States of America
105
28
DOI
出版ステータスPublished - 2008 7 15

ASJC Scopus subject areas

  • 一般

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