PT  - JOURNAL ARTICLE
AU  - Michiko Mori
AU  - Cecilia Andersson
AU  - Medya Shikhagaie
AU  - Anders Bergqvist
AU  - Claes-Göran Löfdahl
AU  - Jonas Erjefält
TI  - LSC 2014 abstract - Expansion of multiple dendritic cell populations in the alveolar parenchyma in patients with COPD
DP  - 2014 Sep 01
TA  - European Respiratory Journal
PG  - P836
VI  - 44
IP  - Suppl 58
4099  - http://erj.ersjournals.com/content/44/Suppl_58/P836.short
4100  - http://erj.ersjournals.com/content/44/Suppl_58/P836.full
SO  - Eur Respir J2014 Sep 01; 44
AB  - Rationale: Recent data suggest that alveolar adaptive immune responses are important immunopathological features of COPD. The cellular basis for alveolar antigen uptake remains however poorly investigated, especially in human lungs. This study performs an extensive histological characterization of alveolar dendritic cell (DC) populations and explores if they are abnormally abundant, or phenotypically altered, in patients with COPD.Methods: Double and triple immunohistochemistry for langerin, CD1a, BDCA-2, CD11c, CD68 and CD163 was performed on distal lung tissues from patients with mild, moderate-to-severe, and very severe COPD. Never-smoking and smoking non-COPD subjects served as controls.Results: Four distinct subsets of alveolar DCs were quantified; langerin+, CD1a+ langerin-, BDCA-2+, and CD11c+ CD68- CD163- DCs. Increased numbers of alveolar CD1a+ langerin- (p<0.05) and BDCA-2+ DCs (p<0.001) were observed in advanced COPD compared with never-smoking and smoking controls. In addition, after exclusion of confounding macrophages, the area of alveolar CD11c+ CD68- CD163- immunoreactivity increased in advanced COPD (p<0.01). In the small airways, langerin+ and BDCA-2+ DCs were also significantly increased. Contrasting the small airway DCs, all alveolar DC subsets but BDCA-2+ frequently extended luminal protrusions. Importantly, alveolar and small airway langerin+DCs were phenotypically different and displayed site-specific marker profiles.Conclusion: Multiple alveolar DC populations are expanded in advanced COPD and are likely to contribute to the aggravated distal adaptive immune responses in this disease.