期刊
IMMUNITY
卷 43, 期 1, 页码 175-186出版社
CELL PRESS
DOI: 10.1016/j.immuni.2015.06.021
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资金
- Japan Society for the Promotion of Science
- Program for Improvement of Research Environment for Young Researchers
- Ministry of Education, Culture, Sports, Science and Technology, Japan
- Ministry of Health, Labour and Welfare, Japan
- Banyu Life Science Foundation International
- Swiss National Science Foundation [320030-140772]
- NIH [AI070813, AI023990, CA072074, U19AI104209]
- MRC [MC_U105178805] Funding Source: UKRI
- Medical Research Council [MC_U105178805] Funding Source: researchfish
- Grants-in-Aid for Scientific Research [15H05786, 15H02515, 15H04866, 15K09560, 15K15377, 15H01267, 15H01162] Funding Source: KAKEN
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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