期刊
NATURE IMMUNOLOGY
卷 10, 期 5, 页码 496-503出版社
NATURE PORTFOLIO
DOI: 10.1038/ni.1719
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资金
- US National Institutes of Health [AI070973, HL082487, AI071130, AR050772, HL075243, AI057696]
- American Lung Association
- Leukemia and Lymphoma Society
- MD Anderson Cancer Center
- Office Of The Director
- EPSCoR [0814442] Funding Source: National Science Foundation
The innate immune response of airway epithelial cells to airborne allergens initiates the development of T cell responses that are central to allergic inflammation. Although proteinase allergens induce the expression of interleukin 25, we show here that epithelial matrix metalloproteinase 7 (MMP7) was expressed during asthma and was required for the maximum activity of interleukin 25 in promoting the differentiation of T helper type 2 cells. Allergen-challenged Mmp7(-/-) mice had less airway hyper-reactivity and production of allergic inflammatory cytokines and higher expression of retinal dehydrogenase 1. Inhibition of retinal dehydrogenase 1 restored the asthma phenotype of Mmp7(-/-) mice and inhibited the responses of lung regulatory T cells, whereas exogenous administration of retinoic acid attenuated the asthma phenotype. Thus, MMP7 coordinates allergic lung inflammation by activating interleukin 25 while simultaneously inhibiting retinoid-dependent development of regulatory T cells.
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