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Lung myeloid dendritic cells coordinately induce TH1 and TH17 responses in human emphysema.

Abstract：

:Exposure to tobacco smoke activates innate and adaptive immune responses that in long-term smokers have been linked to diseases of the lungs, cardiovascular system, joints, and other organs. The destruction of lung tissue that underlies smoking-induced emphysema has been associated with T helper 1 cells that recognize the matrix protein elastin. Factors that result in the development of such autoreactive T cells in smokers remain unknown but are crucial for further understanding the pathogenesis of systemic inflammatory diseases in smokers. Here, we show that lung myeloid dendritic cells were sufficient to induce T helper 1 and T helper 17 responses in CD4 T cells. T helper 1 and 17 cells are invariably present in lungs from patients with emphysema but not in lungs from normal individuals. Interleukin-17A, a canonical T helper 17 cytokine, enhanced secretion of CCL20, a chemoattractant for dendritic cells, and matrix metalloproteinase 12, a potent elastolytic proteinase, from lung macrophages. Thus, although diverse lung factors potentially contribute to T helper effector differentiation in vivo, lung myeloid dendritic cells direct the generation of pathogenic T cells and support a feedback mechanism that sustains both inflammatory cell recruitment and lung destruction. This mechanism may underlie disease in other elastin-rich organs and tissues.

journal_name

Sci Transl Med

journal_title

Science translational medicine

authors

Shan M,Cheng HF,Song LZ,Roberts L,Green L,Hacken-Bitar J,Huh J,Bakaeen F,Coxson HO,Storness-Bliss C,Ramchandani M,Lee SH,Corry DB,Kheradmand F

doi

10.1126/scitranlsmed.3000154

subject

Has Abstract

pub_date

2009-10-28 00:00:00

pages

4ra10

issue

4

eissn

1946-6234

issn

1946-6242

pii

1/4/4ra10

journal_volume

1

pub_type

杂志文章

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