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) 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.
| Original language | English |
|---|---|
| Pages (from-to) | 175-186 |
| Number of pages | 12 |
| Journal | Immunity |
| Volume | 43 |
| Issue number | 1 |
| DOIs | |
| Publication status | Published - 2015 Jul 21 |
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ASJC Scopus subject areas
- Immunology and Allergy
- Infectious Diseases
- Immunology
Cite this
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.
In: Immunity, Vol. 43, No. 1, 21.07.2015, p. 175-186.Research output: Contribution to journal › Article
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TY - JOUR
T1 - An Interleukin-33-Mast Cell-Interleukin-2 Axis Suppresses Papain-Induced Allergic Inflammation By Promoting Regulatory T Cell Numbers
AU - Morita, Hideaki
AU - Arae, Ken
AU - Unno, Hirotoshi
AU - Miyauchi, Kousuke
AU - Toyama, Sumika
AU - Nambu, Aya
AU - Oboki, Keisuke
AU - Ohno, Tatsukuni
AU - Motomura, Kenichiro
AU - Matsuda, Akira
AU - Yamaguchi, Sachiko
AU - Narushima, Seiko
AU - Kajiwara, Naoki
AU - Iikura, Motoyasu
AU - Suto, Hajime
AU - McKenzie, Andrew N J
AU - Takahashi, Takao
AU - Karasuyama, Hajime
AU - Okumura, Ko
AU - Azuma, Miyuki
AU - Moro, Kazuyo
AU - Akdis, Cezmi A.
AU - Galli, Stephen J.
AU - Koyasu, Shigeo
AU - Kubo, Masato
AU - Sudo, Katsuko
AU - Saito, Hirohisa
AU - Matsumoto, Kenji
AU - Nakae, Susumu
PY - 2015/7/21
Y1 - 2015/7/21
N2 - 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.
AB - 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.
UR - http://www.scopus.com/inward/record.url?scp=84937697152&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84937697152&partnerID=8YFLogxK
U2 - 10.1016/j.immuni.2015.06.021
DO - 10.1016/j.immuni.2015.06.021
M3 - Article
C2 - 26200013
AN - SCOPUS:84937697152
VL - 43
SP - 175
EP - 186
JO - Immunity
JF - Immunity
SN - 1074-7613
IS - 1
ER -