共 103 条
Chronic Obstructive Pulmonary Disease 1 New insights into the immunology of chronic obstructive pulmonary disease
被引:562
作者:

Brusselle, Guy G.
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机构:
Ghent Univ Hosp, Lab Translat Res Obstruct Pulm Dis, Dept Resp Med, B-9000 Ghent, Belgium
Univ Ghent, B-9000 Ghent, Belgium Ghent Univ Hosp, Lab Translat Res Obstruct Pulm Dis, Dept Resp Med, B-9000 Ghent, Belgium

Joos, Guy F.
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机构:
Ghent Univ Hosp, Lab Translat Res Obstruct Pulm Dis, Dept Resp Med, B-9000 Ghent, Belgium
Univ Ghent, B-9000 Ghent, Belgium Ghent Univ Hosp, Lab Translat Res Obstruct Pulm Dis, Dept Resp Med, B-9000 Ghent, Belgium

Bracke, Ken R.
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h-index: 0
机构:
Ghent Univ Hosp, Lab Translat Res Obstruct Pulm Dis, Dept Resp Med, B-9000 Ghent, Belgium
Univ Ghent, B-9000 Ghent, Belgium Ghent Univ Hosp, Lab Translat Res Obstruct Pulm Dis, Dept Resp Med, B-9000 Ghent, Belgium
机构:
[1] Ghent Univ Hosp, Lab Translat Res Obstruct Pulm Dis, Dept Resp Med, B-9000 Ghent, Belgium
[2] Univ Ghent, B-9000 Ghent, Belgium
来源:
关键词:
HISTONE DEACETYLASE ACTIVITY;
DENDRITIC CELLS;
INDUCED SPUTUM;
AIRWAY INFLAMMATION;
SYSTEMIC INFLAMMATION;
EXTRACELLULAR-MATRIX;
PERIPHERAL AIRWAYS;
LYMPHOID FOLLICLES;
ADAPTIVE IMMUNITY;
NATURAL-HISTORY;
D O I:
10.1016/S0140-6736(11)60988-4
中图分类号:
R5 [内科学];
学科分类号:
1002 ;
100201 ;
摘要:
Chronic obstructive pulmonary disease (COPD) is a heterogeneous syndrome associated with abnormal inflammatory immune responses of the lung to noxious particles and gases. Cigarette smoke activates innate immune cells such as epithelial cells and macrophages by triggering pattern recognition receptors, either directly or indirectly via the release of damage-associated molecular patterns from stressed or dying cells. Activated dendritic cells induce adaptive immune responses encompassing T helper (Th1 and Th17) CD4+ T cells, CD8+ cytotoxicity, and B-cell responses, which lead to the development of lymphoid follicles on chronic inflammation. Viral and bacterial infections not only cause acute exacerbations of COPD, but also amplify and perpetuate chronic inflammation in stable COPD via pathogen-associated molecular patterns. We discuss the role of autoimmunity (autoantibodies), remodelling, extracellular matrix-derived fragments, impaired innate lung defences, oxidative stress, hypoxia, and dysregulation of microRNAs in the persistence of the pulmonary inflammation despite smoking cessation.
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页码:1015 / 1026
页数:12
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