A novel subset of mouse NKT cells bearing the IL-17 receptor B responds to IL-25 and contributes to airway hyperreactivity

Asuka Terashima, Hiroshi Watarai, Sayo Inoue, Etsuko Sekine, Ryusuke Nakagawa, Koji Hase, Chiaki Iwamura, Hiroshi Nakajima, Toshinori Nakayama, Masaru Taniguchi

研究成果: Article査読

193 被引用数 (Scopus)

抄録

Airway hypersensitive reaction (AHR) is an animal model for asthma, which is caused or enhanced by environmental factors such as allergen exposure. However, the precise mechanisms that drive AHR remain unclear. We identified a novel subset of natural killer T (NKT) cells that expresses the interleukin 17 receptor B (IL-17RB) for IL-25 (also known as IL-17E) and is essential for the induction of AHR. IL-17RB is preferentially expressed on a fraction of CD4 + NKT cells but not on other splenic leukocyte populations tested. IL-17RB+ CD4+ NKT cells produce predominantly IL-13 and Th2 chemokines upon stimulation with IL-25 in vitro. IL-17RB+ NKT cells were detected in the lung, and depletion of IL-17RB+ NKT cells by IL-17RB-specific monoclonal antibodies or NKT cell- deficient Jα18-/- mice failed to develop IL-25-dependent AHR. Cell transfer of IL-17RB+ but not IL-17RB" NKT cells into Jαa18-/- mice also successfully reconstituted AHR induction. These results strongly suggest that IL-17RB + CD4+ NKT cells play a crucial role in the pathogenesis of asthma.

本文言語English
ページ(範囲)2727-2733
ページ数7
ジャーナルJournal of Experimental Medicine
205
12
DOI
出版ステータスPublished - 2008 11 12
外部発表はい

ASJC Scopus subject areas

  • 免疫アレルギー学
  • 免疫学

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