The dendritic cell niche in chronic obstructive pulmonary disease

Respiratory Research

Angela Haczku¹ 

[1] Pulmonary, Allergy and Critical Care Division, Translational Research Laboratories, 125 South 31st Street, Philadelphia, PA 19104-3403, USA

关键词: Mice;    Cigarette smoke exposure;    IL-1α;    IL-1R1;    Dendritic cells;    COPD;   

Others  :  796655
DOI  :  10.1186/1465-9921-13-80

 received in 2012-08-29, accepted in 2012-09-12,  发布年份 2012

【 摘 要 】

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.

【 授权许可】

   
2012 Haczku; licensee BioMed Central Ltd.

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