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An Interleukin-33-Mast Cell-Interleukin-2 Axis Suppresses Papain-Induced Allergic Inflammation by Promoting Regulatory T Cell Numbers.
Morita, Hideaki; Arae, Ken; Unno, Hirotoshi; Miyauchi, Kousuke; Toyama, Sumika; Nambu, Aya; Oboki, Keisuke; Ohno, Tatsukuni; Motomura, Kenichiro; Matsuda, Akira; Yamaguchi, Sachiko; Narushima, Seiko; Kajiwara, Naoki; Iikura, Motoyasu; Suto, Hajime; McKenzie, Andrew N J; Takahashi, Takao; Karasuyama, Hajime; Okumura, Ko; Azuma, Miyuki; Moro, Kazuyo; Akdis, Cezmi A; Galli, Stephen J; Koyasu, Shigeo; Kubo, Masato; Sudo, Katsuko; Saito, Hirohisa; Matsumoto, Kenji; Nakae, Susumu.
Afiliação
  • Morita H; Department of Allergy and Immunology, National Research Institute for Child Health and Development, Tokyo 157-8535, Japan; Department of Pediatrics, Keio University School of Medicine, Tokyo, 160-8582, Japan; Swiss Institute of Allergy and Asthma Research, University of Zurich, Davos 7270, Switzerla
  • Arae K; Department of Allergy and Immunology, National Research Institute for Child Health and Development, Tokyo 157-8535, Japan; Department of Immunology, Faculty of Health Science, Kyorin University, Tokyo, 192-8508, Japan.
  • Unno H; Department of Allergy and Immunology, National Research Institute for Child Health and Development, Tokyo 157-8535, Japan; Department of Pediatrics, The Jikei University School of Medicine, Tokyo 105-8461, Japan.
  • Miyauchi K; Laboratory for Cytokine Regulation, Center for Integrative Medical Sciences, RIKEN Yokohama Institute, Kanagawa 230-0045, Japan.
  • Toyama S; Department of Allergy and Immunology, National Research Institute for Child Health and Development, Tokyo 157-8535, Japan; Department of Immune Regulation, Graduate School of Medical and Dental Science, Tokyo Medical and Dental University, Tokyo 113-8510, Japan.
  • Nambu A; Laboratory of Systems Biology, Center for Experimental Medicine and Systems Biology, The Institute of Medical Science, The University of Tokyo, Tokyo, 108-8639, Japan; Atopy Research Center, Juntendo University School of Medicine, Tokyo 113-8421, Japan.
  • Oboki K; Department of Allergy and Immunology, National Research Institute for Child Health and Development, Tokyo 157-8535, Japan.
  • Ohno T; Department of Allergy and Immunology, National Research Institute for Child Health and Development, Tokyo 157-8535, Japan; Department of Molecular Immunology, Graduate School of Medical and Dental Science, Tokyo Medical and Dental University, Tokyo 113-8510, Japan.
  • Motomura K; Department of Allergy and Immunology, National Research Institute for Child Health and Development, Tokyo 157-8535, Japan.
  • Matsuda A; Department of Ophthalmology, Juntendo University School of Medicine, Tokyo 113-8421, Japan.
  • Yamaguchi S; Laboratory of Systems Biology, Center for Experimental Medicine and Systems Biology, The Institute of Medical Science, The University of Tokyo, Tokyo, 108-8639, Japan.
  • Narushima S; Laboratory of Systems Biology, Center for Experimental Medicine and Systems Biology, The Institute of Medical Science, The University of Tokyo, Tokyo, 108-8639, Japan.
  • Kajiwara N; Department of Allergy and Immunology, National Research Institute for Child Health and Development, Tokyo 157-8535, Japan.
  • Iikura M; Department of Respiratory Medicine, National Center for Global Health and Medicine, Tokyo 162-8655, Japan.
  • Suto H; Atopy Research Center, Juntendo University School of Medicine, Tokyo 113-8421, Japan.
  • McKenzie AN; MRC Laboratory of Molecular Biology, Cambridge CB2 2QH, UK.
  • Takahashi T; Department of Pediatrics, Keio University School of Medicine, Tokyo, 160-8582, Japan.
  • Karasuyama H; Department of Immune Regulation, Graduate School of Medical and Dental Science, Tokyo Medical and Dental University, Tokyo 113-8510, Japan; Japan Science and Technology Agency, Core Research for Evolutional Science and Technology (CREST), Japan Science and Technology Agency, Saitama 332-0012, Japan.
  • Okumura K; Atopy Research Center, Juntendo University School of Medicine, Tokyo 113-8421, Japan.
  • Azuma M; Department of Molecular Immunology, Graduate School of Medical and Dental Science, Tokyo Medical and Dental University, Tokyo 113-8510, Japan.
  • Moro K; Laboratory for Immune Cell System, Center for Integrative Medical Sciences, RIKEN Yokohama Institute, Kanagawa 230-0045, Japan; Precursory Research for Embryonic Science and Technology (PRESTO), Japan Science and Technology Agency, Saitama 332-0012, Japan.
  • Akdis CA; Swiss Institute of Allergy and Asthma Research, University of Zurich, Davos 7270, Switzerland; Christine Kühne-Center for Allergy Research and Education, Davos 7270, Switzerland.
  • Galli SJ; Departments of Pathology and of Microbiology and Immunology, Stanford University School of Medicine, Stanford, CA 94305-5324, USA.
  • Koyasu S; Laboratory for Immune Cell System, Center for Integrative Medical Sciences, RIKEN Yokohama Institute, Kanagawa 230-0045, Japan.
  • Kubo M; Laboratory for Cytokine Regulation, Center for Integrative Medical Sciences, RIKEN Yokohama Institute, Kanagawa 230-0045, Japan; Division of Molecular Pathology, Research Institute for Biological Sciences, Tokyo University of Sciences, Chiba 278-0022, Japan.
  • Sudo K; Animal Research Center, Tokyo Medical University, Tokyo 160-8402, Japan.
  • Saito H; Department of Allergy and Immunology, National Research Institute for Child Health and Development, Tokyo 157-8535, Japan.
  • Matsumoto K; Department of Allergy and Immunology, National Research Institute for Child Health and Development, Tokyo 157-8535, Japan.
  • Nakae S; Department of Allergy and Immunology, National Research Institute for Child Health and Development, Tokyo 157-8535, Japan; Laboratory of Systems Biology, Center for Experimental Medicine and Systems Biology, The Institute of Medical Science, The University of Tokyo, Tokyo, 108-8639, Japan; Precursor
Immunity ; 43(1): 175-86, 2015 Jul 21.
Article em En | MEDLINE | ID: mdl-26200013
ABSTRACT
House dust mite-derived proteases contribute to allergic disorders in part by disrupting epithelial barrier function. Interleukin-33 (IL-33), produced by lung cells after exposure to protease allergens, can induce innate-type airway eosinophilia by activating natural helper (NH) cells, a member of group 2 innate lymphoid cells (ILC2), to secrete Th2 type-cytokines. Because IL-33 also can induce mast cells (MCs) to secrete Th2 type-cytokines, MCs are thought to cooperate with NH cells in enhancing protease or IL-33-mediated innate-type airway eosinophilia. However, we found that MC-deficient Kit(W-sh/W-sh) mice exhibited exacerbated protease-induced lung inflammation associated with reduced numbers of regulatory T (Treg) cells. Moreover, IL-2 produced by IL-33-stimulated MCs promoted expansion of numbers of Treg cells, thereby suppressing development of papain- or IL-33-induced airway eosinophilia. We have thus identified a unique anti-inflammatory pathway that can limit induction of innate-type allergic airway inflammation mediated by NH cells.
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Texto completo: 1 Bases de dados: MEDLINE Assunto principal: Interleucinas / Interleucina-2 / Linfócitos T Reguladores / Inflamação / Mastócitos Tipo de estudo: Prognostic_studies Limite: Animals / Humans Idioma: En Revista: Immunity Assunto da revista: ALERGIA E IMUNOLOGIA Ano de publicação: 2015 Tipo de documento: Article
Texto completo
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Texto completo: 1 Bases de dados: MEDLINE Assunto principal: Interleucinas / Interleucina-2 / Linfócitos T Reguladores / Inflamação / Mastócitos Tipo de estudo: Prognostic_studies Limite: Animals / Humans Idioma: En Revista: Immunity Assunto da revista: ALERGIA E IMUNOLOGIA Ano de publicação: 2015 Tipo de documento: Article