Interleukin-33 in allergy

Authors

  • Tatsukuni Ohno,

    1. Department of Molecular Immunology, Graduate School of Medical and Dental Science, Tokyo Medical and Dental University, Tokyo, Japan
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    • T.O. and H.M. contributed equally to this work.
  • Hideaki Morita,

    1. Department of Pediatrics, Keio University School of Medicine, Tokyo, Japan
    2. Department of Allergy and Immunology, National Research Institute for Child Health & Development, Tokyo, Japan
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    • T.O. and H.M. contributed equally to this work.
  • Ken Arae,

    1. Department of Allergy and Immunology, National Research Institute for Child Health & Development, Tokyo, Japan
    2. Department of Immunology, Faculty of Health Sciences, Kyorin University, Tokyo, Japan
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  • Kenji Matsumoto,

    1. Department of Allergy and Immunology, National Research Institute for Child Health & Development, Tokyo, Japan
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  • Susumu Nakae

    Corresponding author
    1. Laboratory of Systems Biology, Center for Experimental Medicine and Systems Biology, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan
    2. Precursory Research for Embryonic Science and Technology (PRESTO), Japan Science and Technology Agency, Saitama, Japan
    • Department of Molecular Immunology, Graduate School of Medical and Dental Science, Tokyo Medical and Dental University, Tokyo, Japan
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Correspondence

Susumu Nakae, PhD, Laboratory of Systems Biology, Center for Experimental Medicine and Systems Biology, The Institute of Medical Science, The University of Tokyo, 4-6-1 Shirokanedai, Minato-ku, Tokyo, 108-8639, Japan.

Tel.: +81 3 6409 2111

Fax: +81 3 6409 2109

E-mail: snakae@ims.u-tokyo.ac.jp

Abstract

Interleukin-33 (IL-33) is a member of the IL-1 cytokine family, which includes IL-1 and IL-18, and is considered to be important for host defense against nematodes by inducing Th2 cytokine production via the IL-33 receptor. IL-33 receptor is a heterodimer of IL-1 receptor-like 1 (IL-1RL1; also called ST2, T1, Der4, and fit-1) and IL-1 receptor accessory protein (IL-1RAcP). On the other hand, excessive and/or inappropriate production of IL-33 is considered to be involved in the development of various disorders, such as allergic and autoimmune diseases. Unlike IL-1β and IL-18, IL-33 does not seem to be secreted through the activation of inflammasomes in events such as apoptosis. However, IL-33 is localized in the nucleus of cells and is released during tissue injury associated with necrosis. This suggests that it acts as an alarmin, like IL-1α and high-mobility group box chromosomal protein-1 (HMGB-1). This review summarizes current knowledge regarding the roles of IL-33 in the functions of various cell types and the pathogenesis of allergy.

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