期刊
JOURNAL OF CLINICAL IMMUNOLOGY
卷 28, 期 2, 页码 147-156出版社
SPRINGER/PLENUM PUBLISHERS
DOI: 10.1007/s10875-007-9149-0
关键词
dendritic cells; bronchial epithelial cells; diesel exhaust particles; thymic stromal lymphopoietin; lung
类别
资金
- NCRR NIH HHS [M01RR00096, M01 RR000096-380585, M01 RR000096] Funding Source: Medline
- NIAID NIH HHS [AI44729, AI27742-129007] Funding Source: Medline
- NIEHS NIH HHS [R01 ES010187, ES010187, R01 ES010187-08, R01 ES010187-07, T32 ES007267, T32 ES007267-13] Funding Source: Medline
Human exposure to air pollutants, including ambient particulate matter, has been proposed as a mechanism for the rise in allergic disorders. Diesel exhaust particles, a major component of ambient particulate matter, induce sensitization to neoallergens, but the mechanisms by which sensitization occur remain unclear. We show that diesel exhaust particles upregulate thymic stromal lymphopoietin in human bronchial epithelial cells in an oxidant-dependent manner. Thymic stromal lymphopoietin induced by diesel exhaust particles was associated with maturation of myeloid dendritic cells, which was blocked by anti-thymic stromal lymphopoietin antibodies or silencing epithelial cell-derived thymic stromal lymphopoietin. Dendritic cells exposed to diesel exhaust particle-treated human bronchial epithelial cells induced Th2 polarization in a thymic stromal lymphopoietin-dependent manner. These findings provide new insight into the mechanisms by which diesel exhaust particles modify human lung mucosal immunity.
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