4.3 Article

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

期刊

IMMUNOBIOLOGY
卷 218, 期 2, 页码 225-231

出版社

ELSEVIER GMBH, URBAN & FISCHER VERLAG
DOI: 10.1016/j.imbio.2012.04.012

关键词

Airway epithelium; Bronchoalveolar lavage; Chronic bronchitis; Ex-smokers; Regulatory T cell

资金

  1. Swedish Heart-Lung Foundation
  2. King Oscar II Jubilee Foundation
  3. Mats Kleeberg Foundation
  4. King Gustaf V's and Queen Victoria's Freemasons' Foundation
  5. Hesselmans Foundation
  6. Karolinska Institutet
  7. Swedish Research Council
  8. Stockholm County Council

向作者/读者索取更多资源

T cells are accumulated in the lungs of chronic obstructive pulmonary disease (COPD) patients. Intraepithelial T cells, expressing the integrin alpha E (CD103) beta 7, 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 land 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. (C) 2012 Elsevier GmbH. All rights reserved.

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