Epithelial Cell-Derived IL-25, but Not Th17 Cell-Derived IL-17 or IL-17F, Is Crucial for Murine Asthma
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- Maho Suzukawa
- Department of Internal Medicine, Teikyo University School of Medicine , Tokyo 173-8605,
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- Hideaki Morita
- Department of Allergy and Immunology, National Research Institute for Child Health and Development , Tokyo 157-8535,
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- Aya Nambu
- Laboratory of Systems Biology, Center for Experimental Medicine and Systems Biology, The Institute of Medical Science, The University of Tokyo , Tokyo 108-8639,
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- Ken Arae
- Department of Allergy and Immunology, National Research Institute for Child Health and Development , Tokyo 157-8535,
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- Eri Shimura
- Atopy Research Center, Juntendo University School of Medicine , Tokyo 113-8421,
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- Akiko Shibui
- Department of Medical Genomics, Graduate School of Frontier Sciences, The University of Tokyo , Chiba 278-0022,
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- Sachiko Yamaguchi
- Frontier Research Initiative, The Institute of Medical Science, The University of Tokyo , Tokyo 108-8639,
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- Keigo Suzukawa
- Department of Otolaryngology Head and Neck Surgery, The University of Tokyo , Tokyo 113-8655,
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- Wakako Nakanishi
- Department of Otolaryngology Head and Neck Surgery, The University of Tokyo , Tokyo 113-8655,
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- Keisuke Oboki
- Department of Allergy and Immunology, National Research Institute for Child Health and Development , Tokyo 157-8535,
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- Naoki Kajiwara
- Department of Allergy and Immunology, National Research Institute for Child Health and Development , Tokyo 157-8535,
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- Tatsukuni Ohno
- Department of Allergy and Immunology, National Research Institute for Child Health and Development , Tokyo 157-8535,
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- Akina Ishii
- Department of Allergy and Immunology, National Research Institute for Child Health and Development , Tokyo 157-8535,
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- Heinrich Körner
- Menzies Research Institute , Hobart, Tas 7000,
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- Daniel J Cua
- Merck Research Laboratories , Palo Alto, CA 94304
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- Hajime Suto
- Atopy Research Center, Juntendo University School of Medicine , Tokyo 113-8421,
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- Takayuki Yoshimoto
- Intractable Immune System Disease Research Center, Tokyo Medical University , Tokyo 160-8402,
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- Yoichiro Iwakura
- Laboratory of Molecular Pathogenesis, Center for Experimental Medicine and Systems Biology, The Institute of Medical Science, The University of Tokyo , Tokyo 108-8639,
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- Tatsuya Yamasoba
- Department of Otolaryngology Head and Neck Surgery, The University of Tokyo , Tokyo 113-8655,
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- Ken Ohta
- Department of Internal Medicine, Teikyo University School of Medicine , Tokyo 173-8605,
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- Katsuko Sudo
- Animal Research Center, Tokyo Medical University , Tokyo 160-8402,
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- Hirohisa Saito
- Department of Allergy and Immunology, National Research Institute for Child Health and Development , Tokyo 157-8535,
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- Ko Okumura
- Atopy Research Center, Juntendo University School of Medicine , Tokyo 113-8421,
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- David H Broide
- Department of Medicine, University of California , San Diego, La Jolla, CA 92037
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- Kenji Matsumoto
- Department of Allergy and Immunology, National Research Institute for Child Health and Development , Tokyo 157-8535,
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- Susumu Nakae
- Laboratory of Systems Biology, Center for Experimental Medicine and Systems Biology, The Institute of Medical Science, The University of Tokyo , Tokyo 108-8639,
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説明
<jats:title>Abstract</jats:title> <jats:p>IL-17A, IL-17F, and IL-25 are ligands for IL-17RA. In the current study, we demonstrated that IL-25–deficient mice—but not IL-17A–, IL-17F–, IL-17A/F–, IL-23p19–, or retinoic acid-related orphan receptor (ROR)-γt–deficient mice—showed significant suppression of 1) the number of eosinophils and the levels of proinflammatory mediators in bronchoalveolar lavage fluids, 2) airway hyperresponsiveness to methacholine, and 3) OVA-specific IgG1 and IgE levels in the serum during OVA-induced Th2-type/eosinophilic airway inflammation. The IL-25 deficiency did not affect lung dendritic cell migration or Ag-specific memory–Th2 cell expansion during Ag sensitization. Adoptive transfer of T cells, mast cells, or bone marrow cells from IL-25–deficient mice revealed that induction of Th2-type/eosinophilic airway inflammation was dependent on activation of lung epithelial cells and eosinophils by IL-25 produced by airway structural cells such as epithelial cells but not by such hematopoietic stem-cell-origin immune cells as T cells and mast cells. Therefore, airway structural cell-derived IL-25—rather than Th17 cell-derived IL-17A and IL-17F—is responsible for induction of local inflammation by promoting activation of lung epithelial cells and eosinophils in the elicitation phase of Th2-type/eosinophilic airway inflammation. It is not required for Ag-specific Th2 cell differentiation in the sensitization phase.</jats:p>
収録刊行物
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- The Journal of Immunology
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The Journal of Immunology 189 (7), 3641-3652, 2012-10-01
Oxford University Press (OUP)