Respiratory Research | |
Imbalance of dendritic cell co-stimulation in COPD | |
Marek Lommatzsch1  J Christian Virchow1  Katharina Garbe1  Kai Bratke1  Martin Ulrich1  Paul Stoll1  | |
[1] Abteilung für Pneumologie und Internistische Intensivmedizin, Zentrum für Innere Medizin, Universität Rostock, Ernst-Heydemann-Str. 6, Rostock, 18057, Germany | |
关键词: Emphysema; Chronic inflammation; Dendritic cells; COPD; | |
Others : 1133501 DOI : 10.1186/s12931-015-0174-x |
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received in 2014-09-18, accepted in 2015-01-19, 发布年份 2015 |
【 摘 要 】
Background
Dendritic cells (DCs) control immunity and play a role in the pathogenesis of chronic obstructive pulmonary disease (COPD). However, the expression of function-associated surface molecules on circulating DCs in COPD is unknown.
Methods
Four-colour flow cytometry was used to compare blood DC surface molecules of 54 patients with COPD (median age: 59 years; median FEV1: 38% predicted, median CAT score: 24) with two age-matched control groups with normal lung function: 21 current smokers and 21 never-smokers.
Results
Concentrations of plasmacytoid DCs (pDCs) and myeloid DCs (mDCs) and the mDC/pDC ratio did not differ between the groups. The increased expression of BDCA-1, BDCA-3, CD86 and CCR5 on mDCs in patients with COPD did not significantly differ from smokers with normal lung function. In contrast, COPD was specifically characterised by a decreased expression of the anti-inflammatory co-stimulatory molecule PD-L1 on pDCs and an increased expression of the pro-inflammatory co-stimulatory molecule OX40 ligand (OX40L) on mDCs. These changes were not confined to patients with elevated systemic inflammation markers (leukocytes, c-reactive protein, interleukin-6, fibrinogen). The ratio of OX40L to PD-L1 expression (OX40L/PD-L1 ratio), a quantitative measure of imbalanced DC co-stimulation, correlated with the severity of pulmonary emphysema in patients with COPD.
Conclusion
An imbalance of DC co-stimulation might contribute to the pathogenesis of COPD.
【 授权许可】
2015 Stoll et al.; licensee BioMed Central.
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