The dendritic cell niche in chronic obstructive pulmonary disease

Research output: Contribution to journalComment/debate

6 Citations (Scopus)

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.

Original languageEnglish (US)
Article number80
JournalRespiratory Research
Volume13
DOIs
StatePublished - Sep 19 2012
Externally publishedYes

Fingerprint

Dendritic Cells
Chronic Obstructive Pulmonary Disease
T-Lymphocytes
Smoke
Tobacco Products
Lung
Neutrophils
Macrophages
Inflammation
Interleukin-1
Research
Cell Movement
Immune System
Homeostasis

Keywords

  • Cigarette smoke exposure
  • COPD
  • Dendritic cells
  • IL-1α
  • IL-1R1
  • Mice

ASJC Scopus subject areas

  • Pulmonary and Respiratory Medicine

Cite this

The dendritic cell niche in chronic obstructive pulmonary disease. / Haczku, Angela Franciska.

In: Respiratory Research, Vol. 13, 80, 19.09.2012.

Research output: Contribution to journalComment/debate

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