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Published online before print September 19, 2007

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(Journal of Leukocyte Biology. 2007;82:1481-1490.)
© 2007 by Society for Leukocyte Biology

IL-33 induces IL-13 production by mouse mast cells independently of IgE-FcRI signals

Lien H. Ho^*,1, Tatsukuni Ohno^,#,1, Keisuke Oboki, Naoki Kajiwara, Hajime Suto^*,, Motoyasu Iikura^*,||, Yoshimichi Okayama, Shizuo Akira^¶, Hirohisa Saito^,, Stephen J. Galli^*,2 and Susumu Nakae^*,,3

^* Department of Pathology, Stanford University School of Medicine, Stanford, California, USA;
^# Department of Dental Anesthesiology, Tokyo Dental College, Chiba, Japan;
Department of Allergy and Immunology, National Research Institute for Child Health and Development, Tokyo, Japan;
Division of Molecular Cell Immunology and Allergology, Advanced Medical Research Center, Nihon University Graduate School of Medical Sciences, Tokyo, Japan;
Atopy Research Center, Juntendo University, Tokyo, Japan;
^|| Department of Respiratory Medicine, National Disaster Medical Center of Japan, Tokyo, Japan; and
^¶ Department of Host Defense, Research Institute for Microbial Diseases, Osaka University, Osaka, Japan

²Correspondence: Department of Pathology, L-235, Stanford University School of Medicine, 300 Pasteur Drive, Stanford, CA 94305-5324, USA. E-mail: sgalli{at}stanford.edu

The IL-1-related molecules, IL-1 and IL-18, can promote Th2 cytokine production by IgE/antigen-FcRI-stimulated mouse mast cells. Another IL-1-related molecule, IL-33, was identified recently as a ligand for T1/ST2. Although mouse mast cells constitutively express ST2, the effects of IL-33 on mast cell function are poorly understood. We found that IL-33, but not IL-1β or IL-18, induced IL-13 and IL-6 production by mouse bone marrow-derived, cultured mast cells (BMCMCs) independently of IgE. In BMCMCs incubated with the potently cytokinergic SPE-7 IgE without specific antigen, IL-33, IL-1β, and IL-18 each promoted IL-13 and IL-6 production, but the effects of IL-33 were more potent than those of IL-1β or IL-18. IL-33 promoted cytokine production via a MyD88-dependent but Toll/IL-1R domain-containing adaptor-inducing IFN-β-independent pathway. By contrast, IL-33 neither induced nor enhanced mast cell degranulation. At 200 ng/ml, IL-33 prolonged mast cell survival in the absence of IgE and impaired survival in the presence of SPE-7 IgE, whereas at 100 ng/ml, IL-33 had no effect on mast cell survival in the absence of IgE and reduced mast cell survival in the presence of IgE. These observations suggest potential roles for IL-33 in mast cell- and Th2 cytokine-associated immune responses and disorders.

Key Words: cytokines • Fc receptors • mast cells/basophils • allergy

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