An Interleukin-33-Mast Cell-Interleukin-2 Axis Suppresses Papain-Induced Allergic Inflammation By Promoting Regulatory T Cell Numbers

Hideaki Morita, Ken Arae, Hirotoshi Unno, Kousuke Miyauchi, Sumika Toyama, Aya Nambu, Keisuke Oboki, Tatsukuni Ohno, Kenichiro Motomura, Akira Matsuda, Sachiko Yamaguchi, Seiko Narushima, Naoki Kajiwara, Motoyasu Iikura, Hajime Suto, Andrew N.J. McKenzie, Takao Takahashi, Hajime Karasuyama, Ko Okumura, Miyuki AzumaKazuyo Moro, Cezmi A. Akdis, Stephen J. Galli, Shigeo Koyasu, Masato Kubo, Katsuko Sudo, Hirohisa Saito, Kenji Matsumoto, Susumu Nakae

研究成果: Article

141 被引用数 (Scopus)

抄録

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) tosecrete Th2 type-cytokines, MCs are thought tocooperate with NH cells in enhancing protease orIL-33-mediated innate-type airway eosinophilia. However, we found that MC-deficient KitW-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.

本文言語English
ページ(範囲)175-186
ページ数12
ジャーナルImmunity
43
1
DOI
出版ステータスPublished - 2015 7 21

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology
  • Infectious Diseases

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