title: Imbalance between subpopulations of regulatory T cells in COPD.
abstract: BACKGROUND
  Recent evidence indicates that human regulatory T cells (Tregs) are composed of three distinct subpopulations: CD25(++) CD45RA(+) resting Tregs (rTregs), CD25(+++) CD45RA(-) activated Tregs (aTregs), which are suppressive, and CD25(++) CD45RA(-) cytokine-secreting (Fr III) cells with pro-inflammatory capacity.
  
  
  OBJECTIVE
  To evaluate the dynamic changes in circulating and pulmonary Treg subpopulations in smokers and patients with chronic obstructive pulmonary disease (COPD), and to explore their potential roles in COPD pathogenesis.
  
  
  METHODS
  Blood samples were obtained from 57 never-smokers, 32 smokers with normal lung function and 66 patients with COPD. Bronchoalveolar lavage (BAL) samples were taken from 12 never-smokers, 12 smokers and 18 patients with COPD. The proportions of Treg subpopulations and activated CD8 T cells were evaluated using flow cytometry.
  
  
  RESULTS
  In peripheral blood, increased proportions of rTregs, aTregs and Fr III cells were found in smokers compared with never-smokers, whereas patients with COPD showed decreased rTregs and aTregs, and significantly increased Fr III cells compared with smokers. The changes in Treg subpopulations, with an overall decrease in the (aTreg+rTreg):(Fr III) ratio, indicated that immune homeostasis favoured inflammation and correlated with enhanced CD8 T-cell activation (r=-0.399, p<0.001) and forced expiratory volume in 1 s (FEV1) % predicted value (r=0.435, p<0.001).The BAL (aTreg+rTreg):(Fr III) ratios displayed more robust correlations with FEV1% predicted value (r=0.741, p<0.01) and activation of effector T cells (r=-0.763, p<0.001).
  
  
  CONCLUSIONS
  The imbalance between the anti-inflammatory subsets (aTreg+rTreg) and the pro-inflammatory subset (Fr III) of Tregs may play an important role in COPD progression.
authors.affiliation: Department of Respiratory Medicine, Beijing Tongren Hospital, Capital Medical University, , Beijing, China.
authors.forename: Jia
authors.initials: J
authors.lastname: Hou
authors.forename: Yongchang
authors.initials: Y
authors.lastname: Sun
authors.forename: Yu
authors.initials: Y
authors.lastname: Hao
authors.forename: Jie
authors.initials: J
authors.lastname: Zhuo
authors.forename: Xiaofang
authors.initials: X
authors.lastname: Liu
authors.forename: Peng
authors.initials: P
authors.lastname: Bai
authors.forename: Junyan
authors.initials: J
authors.lastname: Han
authors.forename: Xiwei
authors.initials: X
authors.lastname: Zheng
authors.forename: Hui
authors.initials: H
authors.lastname: Zeng
mesh_terms: D000368:Aged; D001992:Bronchoalveolar Lavage Fluid / Q000166:cytology; D018414:CD8-Positive T-Lymphocytes; D005260:Female; D005541:Forced Expiratory Volume; D006706:Homeostasis; D006801:Humans; D053645:Interleukin-2 Receptor alpha Subunit / Q000032:analysis*; D017493:Leukocyte Common Antigens / Q000032:analysis*; D008213:Lymphocyte Activation; D018655:Lymphocyte Count; D008297:Male; D008875:Middle Aged; D029424:Pulmonary Disease, Chronic Obstructive / Q000276:immunology* / Q000503:physiopathology; D012720:Severity of Illness Index; D012907:Smoking / Q000276:immunology*; D050378:T-Lymphocytes, Regulatory / Q000737:chemistry / Q000276:immunology*
chemical_list: D053645:Interleukin-2 Receptor alpha Subunit; D017493:Leukocyte Common Antigens
keywords: Bronchoscopy; COPD AU Mechanisms; Lymphocyte Biology