Emerging roles of IL-33 in inflammation and immune regulation

DOI 参考文献95件
  • Ikutani Masashi
    Department of Immunobiology and Pharmacological Genetics, Graduate School of Medicine and Pharmaceutical Science for Research, University of Toyama, Toyama, Japan
  • Tsuneyama Koichi
    Department of Diagnostic Pathology, Graduate School of Medicine and Pharmaceutical Sciences, University of Toyama, Toyama, Japan
  • Nakae Susumu
    Laboratory of Systems Biology, Center for Experimental Medicine and Systems Biology, The Institute of Medical Science, The University of Tokyo, Tokyo, Japan
  • Takatsu Kiyoshi
    Department of Immunobiology and Pharmacological Genetics, Graduate School of Medicine and Pharmaceutical Science for Research, University of Toyama, Toyama, Japan Toyama Prefectural Institute for Pharmaceutical Research, Toyama, Japan

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Interleukin-33 (IL-33) belongs to the IL-1 family of cytokines and has been reported to play multiple roles in host defense, allergies and chronic inflammation. Constitutive expression of IL-33 in epithelial cells ensures rapid immune responses against invading pathogens such as parasites and viruses. Tissue damage caused by pathogens results in the release of extracellular IL-33 that in turn alerts a variety of immune cells such as group 2 innate lymphoid cells (ILC2s), eosinophils, basophils and mast cells. These cells mediate T helper type 2 (Th2) immune responses to destroy pathogens. IL-33 also plays central roles in mediating allergic diseases including asthma and atopic rhinitis. Although the functions of IL-33 in host defense and allergies initially received most attention, focus is turning to its roles in chronic inflammatory diseases. Recent advances, however, have led to problematic results. In addition to Th2 responses, IL-33 also promotes Th1 responses and there have been positive and negative roles reported for IL-33 in inflammatory diseases. This mini-review will summarize IL-33 biology and discuss issues regarding previously unrecognized roles of IL-33.

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