Journal
EUROPEAN JOURNAL OF IMMUNOLOGY
Volume 38, Issue 10, Pages 2751-2761Publisher
WILEY-BLACKWELL
DOI: 10.1002/eji.200838542
Keywords
DC; Immune regulation; Lung inflammation; Treg; Stromal cells
Categories
Funding
- National Key Basic Research Program of China [2007CB512403]
- National Natural Science Foundation of China [30721091, 30731160623]
- Shanghai Committee of Science and Technology [05DZ22106]
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The tissue microenvironment may affect the development and function of immune cells such as DC. Whether and how the pulmonary stromal microenvironment can affect the development and function of lung DC need to be investigated. Regulatory DC (DCreg) can regulate T-cell response. We wondered whether such regulatory DC exist in the lung and what is the effect of the pulmonary stromal microenvironment on the generation of DCreg. Here we demonstrate that murine pulmonary stromal cells can drive immature DC, which are regarded as being widely distributed in the lung, to proliferate and differentiate into a distinct subset of DCreg, which express high levels of CD11b but low levels of MHC class II (I-A), CD11c, secrete high amounts of IL-10, NO and prostaglandin E-2 (PGE(2)) and suppress T-cell proliferation. The natural counterpart of DCreg in the lung with similar phenotype and regulatory function has been identified. Pulmonary stroma-derived TGF-beta is responsible for the differentiation of immature DC to DCreg, and DCreg-derived PGE2 contributes to their suppression of T-cell proliferation. Moreover, DCreg can induce the generation of CD4(+)CD25(+)Foxp3(+) Treg. Importantly, infusion with DCreg attenuates T-cell-mediated eosinophilic airway inflammation in vitro. Therefore, the pulmonary microenvironment may drive the generation of DCreg, thus contributing to the maintenance of immune homoeostasis and the control of inflammation in the lung.
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