Aryl hydrocarbon receptor deficiency in T cells suppresses the development of collagen-induced arthritis

Taisuke Nakahama, Akihiro Kimura, Nam Trung Nguyen, Ichino Chinen, Hamza Hanieh, Keiko Nohara, Yoshiaki Fujii-Kuriyama, Tadamitsu Kishimoto

Research output: Contribution to journalArticlepeer-review

86 Citations (Scopus)

Abstract

The contributions of aryl hydrocarbon receptor (Ahr) to the pathogenesis of rheumatoid arthritis have not been elucidated. Here, we show that Ahr deficiency ameliorated collagen-induced arthritis, a mouse model of RA. Collagen-immunized Ahr KO mice showed decreased serum levels of such proinflammatory cytokines as IL-1β and IL-6. The Th17 and Th1 cell populations in lymph nodes from these mice decreased and increased, respectively, whereas the percentage of regulatory T cells was unchanged. Interestingly, a lack of Ahr specifically in T cells significantly suppressed collagen-induced arthritis development, whereas Ahr deficiency in macrophages had no effect. These finding indicate that the development of experimental autoimmune arthritis depends on the presence of Ahr in T cells, and that Th1/Th17 balance may be particularly important for this process.

Original languageEnglish
Pages (from-to)14222-14227
Number of pages6
JournalProceedings of the National Academy of Sciences of the United States of America
Volume108
Issue number34
DOIs
Publication statusPublished - 2011 Aug 23

Keywords

  • Autoimmunity
  • Dioxin receptor
  • Immune regulation

ASJC Scopus subject areas

  • General

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