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International Immunology, Vol. 15, No. 4, pp. 483-490, April 2003
© 2003 Japanese Society for Immunology

IL-1 is required for allergen-specific Th2 cell activation and the development of airway hypersensitivity response

Susumu Nakae1, Yutaka Komiyama1, Hiroshi Yokoyama1,4, Aya Nambu1, Masaomi Umeda3, Michiko Iwase2, Ikuo Homma2, Katsuko Sudo1, Reiko Horai1, Masahide Asano1,5 and Yoichiro Iwakura1

1 Center for Experimental Medicine, Institute of Medical Science, University of Tokyo, 4-6-1 Shirokanedai, Minato-ku, Tokyo 108-8639, Japan 2 Second Department of Physiology, Showa University School of Medicine, 1-5-8 Hatanodai, Shinagawa-ku, Tokyo 142-8555, Japan 3 Research Center Kyoto, Bayer Yakuhin, Ltd, 6-5-1-3 Kunimidai, Kizu-cho, Sorakugun, Kyoto 619-0216, Japan 4 Present address: Department of Biophysics and Biochemistry, Graduate School of Science, University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-0033, Japan 5 Present address: Institute for Experimental Animals, School of Medicine, Kanazawa University, 13-1 Takaramachi, Kanazawa 920-8640, Japan

Correspondence to: Y. Iwakura; E-mail: iwakura{at}ims.u-tokyo.ac.jp
Transmitting editor: S. J. Galli

IL-1 is a pro-inflammatory cytokine consisted of two molecular species, IL-1{alpha} and IL-1ß, and the IL-1 receptor antagonist (IL-1Ra) is a natural inhibitor of both molecules. Although it is suggested that IL-1 potentiates immune responses mediated by Th2 cells, the role of IL-1 in asthma still remains unclear. In this study, we demonstrate that the ovalbumin (OVA)-induced airway hypersensitivity response (AHR) in IL-1{alpha}/ß-deficient (IL-1{alpha}/ß–/–) mice was significantly reduced from the levels seen in wild-type mice, whereas the responses seen in IL-1Ra–/– mice were profoundly exacerbated, suggesting that IL-1 is required for Th2 cell activation during AHR. OVA-specific T cell proliferation, IL-4 and IL-5 production by T cells, and IgG1 and IgE production by B cells in IL-1{alpha}/ß–/– mice were markedly reduced compared with these responses in wild-type mice; such responses were enhanced in IL-1Ra–/– mice. Using IL-1{alpha}–/– and IL-1ß–/– mice, we determined that both IL-1{alpha} and IL-1ß are involved in this reaction. Both IgG1 and IgE levels were reduced in IL-1ß–/– mice, while only IgE levels were affected in IL-1{alpha}–/– mice, indicating a functional difference between IL-1{alpha} and IL-1ß. These observations indicate that IL-1 plays important roles in the development of AHR.

Keywords: IL-1 receptor antagonist, IL-1{alpha}, IL-1ß, knockout mouse


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