Dendritic cells in pathogenesis of COPD
Masoumeh Ezzati Givi
Frank A. Redegeld
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COPD (Chronic Obstructive Pulmonary Disease) is an important lung and airway disease which affects the lives of around 200 million people worldwide with an increasing incidence particularly in developing countries. The pathogenesis of COPD is based on the innate and adaptive inflammatory immune response to the inhalation of toxic particles and gases. Although cigarette smoking is the primary cause of this inflammation, many other environmental and occupational exposures contribute to the pathology of COPD. The immune inflammatory changes associated with COPD are linked to a tissue repair and remodeling process that increases mucus production and causes emphysematous destruction of the gas-exchanging surface of the lung. The inflamed airways of COPD patients contain several inflammatory cells including neutron phils, macrophages, T lymphocytes, and dendritic cells (DCs). Little is known about the relative contribution of DCs in the pathogenesis of COPD. However the number of DCs is changed in smokers and COPD patients and cigarette smoke (CS) induces the release of chemokines from DCs that play a role in the pathogen esis of COPD. In this review paper, an overview is presented on the role of DCs and their mediators in the pathogenesis of COPD. The activation of DCs and their signaling in response to CS will also be highlighted and discussed. © 2012 Bentham Science Publishers.