Abstract:
:The pulmonary innate immune system is heavily implicated in the perpetual airway inflammation and impaired host defense characterizing Chronic Obstructive Pulmonary Disease (COPD). The airways of patients suffering from COPD are infiltrated by various immune and inflammatory cells including macrophages, neutrophils, T lymphocytes, and dendritic cells. While the role of macrophages, neutrophils and T lymphocytes is well characterized, the contribution of dendritic cells to COPD pathogenesis is still the subject of emerging research. A paper by Botelho and colleagues in the current issue of Respiratory Research investigates the importance of dendritic cell recruitment in cigarette-smoke induced acute and chronic inflammation in mice. Dendritic cells of the healthy lung parenchyma and airways perform an important sentinel function and regulate immune homeostasis. During inflammatory responses the function and migration pattern of these cells is dramatically altered but the underlying mechanisms are incompletely understood. Botelho and colleagues demonstrate here the importance of IL-1R1/IL-1α related mechanisms including CCL20 production in cigarette-smoke induced recruitment of dendritic cells and T cell activation in the mouse lung.
journal_name
Respir Resjournal_title
Respiratory researchauthors
Haczku Adoi
10.1186/1465-9921-13-80subject
Has Abstractpub_date
2012-09-19 00:00:00pages
80eissn
1465-9921issn
1465-993Xpii
1465-9921-13-80journal_volume
13pub_type
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pub_type: 临床试验,杂志文章
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pub_type: 杂志文章,评审
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更新日期:2007-10-04 00:00:00
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pub_type: 杂志文章
doi:10.1186/1465-9921-14-140
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