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Human mast cell activation through Fc receptors and Toll-like receptors

Authors

  • Yoshimichi Okayama,

    1. Reaserch Unit for Allergy Transcriptome, Research Center for Allergy and Immunology, RIKEN Yokohama Institute, Yokohama,
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  • Shigeru Okumura,

    1. Reaserch Unit for Allergy Transcriptome, Research Center for Allergy and Immunology, RIKEN Yokohama Institute, Yokohama,
    2. Department of Microbiology, Tokyo Dental College, Chiba, Japan
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  • Hisashi Tomita,

    1. Reaserch Unit for Allergy Transcriptome, Research Center for Allergy and Immunology, RIKEN Yokohama Institute, Yokohama,
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  • Hiroko Katayama,

    1. Reaserch Unit for Allergy Transcriptome, Research Center for Allergy and Immunology, RIKEN Yokohama Institute, Yokohama,
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  • Keisuke Yuki,

    1. Reaserch Unit for Allergy Transcriptome, Research Center for Allergy and Immunology, RIKEN Yokohama Institute, Yokohama,
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  • Shinji Kagaya,

    1. Reaserch Unit for Allergy Transcriptome, Research Center for Allergy and Immunology, RIKEN Yokohama Institute, Yokohama,
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  • Jun-ichi Kashiwakura,

    1. Reaserch Unit for Allergy Transcriptome, Research Center for Allergy and Immunology, RIKEN Yokohama Institute, Yokohama,
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  • Hirohisa Saito

    1. Reaserch Unit for Allergy Transcriptome, Research Center for Allergy and Immunology, RIKEN Yokohama Institute, Yokohama,
    2. Department of Allergy and Immunology, National Research Institute for Child Health and Development, Tokyo and
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Dr Yoshimichi Okayama, Research Unit for Allergy Transcriptome, Research Center for Allergy and Immunology, RIKEN Yokohama Institute, 1-7-22 Suehiro-cho, Tsurumi-ku, Yokohama, Kanagawa 230-0045, Japan. Email: yokayama@rcai.riken.go.jp

Abstract

Mast cells express high-affinity IgE receptors (FcɛRI) on their surface and can be activated to secrete a variety of biologically active mediators by cross-linking of receptor-bound IgE. Recent studies in animal models indicate that mouse mast cells may play a protective role in host defense against bacteria through the production of tumor necrosis factor-α, mainly as a result of Toll-like receptor (TLR) 4- or CD48-mediated activation. Moreover, several recent observations in animal models have indicated that mast cells may also play a pivotal role in coordinating the early phases of autoimmune diseases, particularly those involving auto-antibodies. We recently identified functional TLR4 and FcγRI on human mast cells, in which their expression had been upregulated by interferon-γ. We compared each of the receptor-mediated gene expression profiles with the FcɛRI-mediated gene expression profile using high-density oligonucleotide probe arrays and discovered that human mast cells may modulate the immune system in a receptor-specific manner.

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