期刊
IMMUNITY
卷 40, 期 5, 页码 758-771出版社
CELL PRESS
DOI: 10.1016/j.immuni.2014.04.013
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资金
- Ministry of Education, Culture, Sports, Science, and Technology (MEXT) of Japan [23118526]
- Japan Society for the Promotion of Science (JSPS) [24249058, 22689013, 22229004]
- Program for Promotion of Fundamental Studies in Health Sciences of the National Institute of Biomedical Innovation (NIBIO)
- Japan Science and Technology Agency (JST)
- Takeda Foundation
- Grants-in-Aid for Scientific Research [25670235, 22229004] Funding Source: KAKEN
Allergic asthma is an inflammatory disease characterized by lung eosinophilia controlled by type 2 cytokines. Cysteine proteases are potent triggers of allergic inflammation by causing barrier disruption in lung epithelial cells inducing the elevation of interleukin-5 (IL-5) and IL-13 from natural helper (NH) cells, a member of ILC2s, which leads to lung eosinophilia. In this study, we found that basophils play a crucial role in NH cell-mediated eosinophilic inflammation induced by protease allergens. Conditional deletion of basophils caused a resolution of the papain-induced eosinophilia and mucus production. Resolution of eosinophilia was also observed in mice lacking IL-4 specifically in basophils, indicating that basophil-derived IL-4 enhanced expression of the chemokine CCL11, as well as IL-5, IL-9, and IL-13 in NH cells, thus attracting eosinophils. These results demonstrate that IL-4 from basophils has an important role in the NH-derived cytokine and chemokine expression, subsequently leading to protease allergen-induced airway inflammation.
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