title: Peripheral Tc17 and Tc17/Interferon-γ Cells are Increased and Associated with Lung Function in Patients with Chronic Obstructive Pulmonary Disease.
abstract: BACKGROUND
  Chronic obstructive pulmonary disease (COPD) is characterized by progressive loss of lung function and local and systemic inflammation, in which CD8+ T-cells are believed to play a key role. Activated CD8+ T-cells differentiate into distinct subpopulations, including interferon-γ (IFN-γ)-producing Tc1 and interleukin (IL)-17-producing Tc17 cells. Recent evidence indicates that Tc17 cells exhibit considerable plasticity and may convert into IL-17/IFN-γ-double producing (Tc17/IFN-γ) cells when driven by inflammatory conditions. The aim of this study was to investigate the Tc17/IFN-γ subpopulation in peripheral blood of patients with COPD and to evaluate their potential roles in this disease.
  
  
  METHODS
  Peripheral blood samples were collected from 15 never-smokers, 23 smokers with normal lung function, and 25 patients with COPD (Global Initiative for Chronic Obstructive Lung Disease 2-4). Proportions of the IL-17/IFN-γ-double expressing subpopulation were assessed using flow cytometry. Plasma concentrations of cytokines favoring Tc17/IFN-γ differentiation were measured by enzyme-linked immunosorbent assay.
  
  
  RESULTS
  Patients with COPD had higher proportions of Tc17 cells and Tc17/IFN-γ cells in the peripheral blood than smokers and never-smokers. The plasticity of Tc17 cells was higher than that of Th17 cells. The percentages of Tc17 cells and Tc17/IFN-γ cells showed negative correlations with forced expiratory volume in 1 s % predicted value (r = -0.418, P = 0.03; r = -0.596, P = 0.002, respectively). The plasma concentrations of IL-6, transforming growth factor-β1, and IL-12 were significantly higher in patients with COPD compared with smokers and never-smokers.
  
  
  CONCLUSIONS
  Peripheral Tc17 cells are increased and more likely to convert to Tc17/IFN-γ cells in COPD, suggesting that Tc17 cell plasticity may be involved in persistent inflammation of the disease.
authors.forename: Wei-Han
authors.initials: WH
authors.lastname: Xu
authors.forename: Xiao-Ling
authors.initials: XL
authors.lastname: Hu
authors.forename: Xiao-Fang
authors.initials: XF
authors.lastname: Liu
authors.forename: Peng
authors.initials: P
authors.lastname: Bai
authors.affiliation: Department of Respiratory Medicine, Beijing Tongren Hospital, Capital Medical University, Beijing 100730; Department of Respiratory and Critical Care Medicine, Peking University Third Hospital, Beijing 100191, China.
authors.forename: Yong-Chang
authors.initials: YC
authors.lastname: Sun
mesh_terms: D000368:Aged; D005260:Female; D005541:Forced Expiratory Volume; D006801:Humans; D007371:Interferon-gamma / Q000096:biosynthesis*; D018664:Interleukin-12 / Q000097:blood; D015850:Interleukin-6 / Q000097:blood; D008168:Lung / Q000503:physiopathology*; D008297:Male; D008875:Middle Aged; D029424:Pulmonary Disease, Chronic Obstructive / Q000276:immunology* / Q000503:physiopathology; D058504:Th17 Cells / Q000276:immunology*
chemical_list: C508600:IL6 protein, human; D015850:Interleukin-6; D018664:Interleukin-12; D007371:Interferon-gamma