RESEARCH n a a in

ial ch sm cells (DCs), which are subdivided into myeloid DCs (mDCs) and plasmacytoid DCs (pDCs), are specialized markers on one cell). For instance, it is currently un-clear whether the decrease in CD83 positive cells in Stoll et al. Respiratory Research 2014, 15:48 http://respiratory-research.com/content/15/1/48etry display a strong upregulation of specific receptors forDepartment of Pneumology and Critical Care Medicine, University of Rostock, Ernst-Heydemann-Str. 6, 18057 Rostock, Germanyantigen-presenting cells which initiate and control adaptive immune responses in the lung. These cells were postulated to play a key role in the formation of lymphoid follicles in small airways of patients with COPD [3-6]. In line with this postulate, histologic stud-ies using lung tissue from patients with COPD showed small airways of patients with COPD represents a de-crease in the total number of DCs or a reduced expres-sion of this maturation marker on DCs [12]. Over the last years, we have established a flow cytometric method to comprehensively analyze function-associated surface molecules on DCs in human bronchoalveolar lavage fluid (BALF) [13-16]. Using this method, we have demon-strated that BALF mDCs of smokers with normal spirom- * Correspondence: marek.lommatzsch@med.uni-rostock.deResults: Myeloid DCs of current smokers with COPD displayed a significantly increased expression of receptors for antigen recognition such as BDCA-1 or Langerin, as compared with never-smoking controls. In contrast, former smokers with COPD displayed a significantly decreased expression of these receptors, as compared with never-smoking controls. A significantly reduced expression of the maturation marker CD83 on myeloid DCs was found in current smokers with COPD, but not in former smokers with COPD. The chemokine receptor CCR5 on myeloid DCs, which is also important for the uptake and procession of microbial antigens, was strongly reduced in all patients with COPD, independently of the smoking status. Conclusion: COPD is characterized by a strongly reduced CCR5 expression on myeloid DCs in the airway lumen, which might hamper DC interactions with microbial antigens. Further studies are needed to better understand the role of CCR5 in the pathophysiology and microbiology of COPD