The Journal of Experimental Medicine
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Published online 14 April 2003 doi:10.1084/jem.20021701
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© Rockefeller University Press, 0022-1007/2003/4/997 $5.00
The Journal of Experimental Medicine, Volume 197, Number 8, 997-1005

Nonredundant Roles for CD1d-restricted Natural Killer T Cells and Conventional CD4+ T Cells in the Induction of Immunoglobulin E Antibodies in Response to Interleukin 18 Treatment of Mice

Tomohiro Yoshimoto1,2, Booki Min3, Takaaki Sugimoto1,2, Nobuki Hayashi1,2, Yuriko Ishikawa1,2, Yuki Sasaki1,2, Hitomi Hata1,2, Kazuyoshi Takeda4, Ko Okumura4, Luc Van Kaer5, William E. Paul3 and Kenji Nakanishi1,2

1 Department of Immunology and Medical Zoology, Hyogo College of Medicine, Nishinomiya, Hyogo 663-8501, Japan
2 Core Research for Evolutional Science and Technology, Japan Science and Technology Corporation, Saitama 332-0012, Japan
3 Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892
4 Department of Immunology, Juntendo University School of Medicine, Tokyo 113-8421, Japan
5 Department of Microbiology and Immunology, Vanderbilt University School of Medicine, Nashville, TN 37232

Address correspondence to Kenji Nakanishi, Department of Immunology and Medical Zoology, Hyogo College of Medicine, 1-1 Mukogawa-cho, Nishinomiya, Hyogo 663-8501, Japan. Phone: 81-798-45-6572; Fax: 81-798-40-5423; E-mail: nakaken{at}hyo-med.ac.jp

Interleukin (IL)-18 synergizes with IL-12 to promote T helper cell (Th)1 responses. Somewhat paradoxically, IL-18 administration alone strongly induces immunoglobulin (Ig)E production and allergic inflammation, indicating a role for IL-18 in the generation of Th2 responses. The ability of IL-18 to induce IgE is dependent on CD4+ T cells, IL-4, and signal transducer and activator of transcription (stat)6. Here, we show that IL-18 fails to induce IgE both in CD1d-/- mice that lack natural killer T (NKT) cells and in class II-/- mice that lack conventional CD4+ T cells. However, class II-/- mice reconstituted with conventional CD4+ T cells show the capacity to produce IgE in response to IL-18. NKT cells express high levels of IL-18 receptor (R){alpha} chain and produce significant amounts of IL-4, IL-9, and IL-13, and induce CD40 ligand expression in response to IL-2 and IL-18 stimulation in vitro. In contrast, conventional CD4+ T cells express low levels of IL-18R{alpha} and poorly respond to IL-2 and IL-18. Nevertheless, conventional CD4+ T cells are essential for B cell IgE responses after the administration of IL-18. These findings indicate that NKT cells might be the major source of IL-4 in response to IL-18 administration and that conventional CD4+ T cells demonstrate their helper function in the presence of NKT cells.

Key Words: IL-18R • CD4+ NK1.1+ T cells • Th2 cytokines • CD40 ligand • allergy


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