The Journal of Experimental Medicine
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doi:10.1084/jem.20080698
The Journal of Experimental Medicine
The Rockefeller University Press, 0022-1007 $30.00
© Terashima et al.
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BRIEF DEFINITIVE REPORT

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

Asuka Terashima1, Hiroshi Watarai1, Sayo Inoue1, Etsuko Sekine1, Ryusuke Nakagawa1, Koji Hase2, Chiaki Iwamura3, Hiroshi Nakajima4, Toshinori Nakayama3, and Masaru Taniguchi1

1 Laboratory for Immune Regulation and 2 Laboratory for Epithelial Immunobiology, RIKEN Research Center for Allergy and Immunology, Tsurumi-ku, Yokohama, Kanagawa, 230-0045, Japan
3 Department of Immunology and 4 Department of Molecular Genetics, Graduate School of Medicine, Chiba University, Chuo-ku, Chiba, 260-8670, Japan

CORRESPONDENCE Hiroshi Watarai: hwatarai{at}rcai.riken.jp

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 J{alpha}18–/– mice failed to develop IL-25–dependent AHR. Cell transfer of IL-17RB+ but not IL-17RB– NKT cells into J{alpha}18–/– 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.

A. Terashima and H. Watarai contributed equally to this paper.

© 2008 Terashima et al. This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.jem.org/misc/terms.shtml). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 3.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/3.0/).


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