Increased intraepithelial (CD103+) CD8+ T cells in the airways of smokers with and without chronic obstructive pulmonary disease

Abstract T cells are accumulated in the lungs of chronic obstructive pulmonary disease (COPD) patients. Intraepithelial T cells, expressing the integrin αE (CD103) β7, and regulatory T cells have been implicated in pathogenesis of the disease. We asked whether COPD patients and smokers have altered...

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Published inImmunobiology (1979) Vol. 218; no. 2; pp. 225 - 231
Main Authors Mikko, M, Forsslund, H, Cui, L, Grunewald, J, Wheelock, Å.M, Wahlström, J, Sköld, C.M
Format Journal Article
LanguageEnglish
Published Netherlands Elsevier GmbH 01.02.2013
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Summary:Abstract T cells are accumulated in the lungs of chronic obstructive pulmonary disease (COPD) patients. Intraepithelial T cells, expressing the integrin αE (CD103) β7, and regulatory T cells have been implicated in pathogenesis of the disease. We asked whether COPD patients and smokers have altered frequencies of these T cells and if their phenotypes differ. A total of 40 never-smokers, 40 smokers with normal lung function and 38 COPD patients (GOLD I and II), of which 11 were ex-smokers, were included. T cells in bronchoalveolar lavage (BAL) fluid and peripheral blood were analysed for the expression of CD103, FOXP3 and markers of activation and differentiation using multi-colour flow cytometry. Smokers, regardless of airway obstruction, had significantly more CD8+CD103+ cells in their BAL fluid compared to never-smokers but less of those cells were CD27 + CD69−. Smokers, in particular those with chronic bronchitis, had a higher percentage of CD4 + FOXP3+ T-regulatory BAL cells compared to never-smokers and COPD ex-smokers. Chronic cigarette smoking leads to an accumulation of CD8+ T cells with an altered phenotype in the airway epithelium. The increased frequency of regulatory T cells may influence the ability to regulate smoke-induced inflammation which could be decisive for disease development. Our results further indicate a reversibility of smoke-induced changes.
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ISSN:0171-2985
1878-3279
1878-3279
DOI:10.1016/j.imbio.2012.04.012