title: Correlation between peripheral blood T-cell profiles and clinical and inflammatory parameters in stable COPD.
abstract: BACKGROUND
  Recent studies suggest that Tc1/Tc2 imbalances are implicated in the pathogenesis of chronic obstructive pulmonary disease (COPD). The purpose of this study was to clarify the relationship between peripheral blood T-cell profiles and pulmonary function or inflammatory parameters.
  
  
  METHODS
  Thirty-one patients with stable COPD (median age 70 years, 30 males, 15 current smokers and 16 ex-smokers) and 30 healthy control subjects were enrolled in this study. The subjects underwent blood tests, exhaled nitric oxide (eNO) measurement, pulmonary function tests, and sputum induction. Tc1/Tc2 and Th1/Th2 were determined by analyzing intracellular cytokine staining for IFN-gamma and IL-4 in peripheral blood CD8+ and CD4+ T cells using flow cytometry after stimulation with phorbol 12-myristate 13-acetate and ionomycin.
  
  
  RESULTS
  There was a significantly increased proportion of IFN-gamma-producing and IL-4-producing CD8+ T cells in patients with COPD compared with control subjects (median [IQR] 73.6% [63.9%-80.7%] vs 62.0% [45.6%-73.8%], p=0.004; and 2.6% [1.1%-6.9%] vs 1.1% [0.6%-2.2%], p=0.002, respectively). In addition, the proportion of IFN-gamma-producing CD4+ T cells was significantly higher in patients with COPD compared with control subjects (25.7% [21.2%-38.0%] vs 22.8% [15.6%-29.2%], p=0.027). The proportion of IFN-gamma-producing CD8+ T cells was correlated negatively with single-breath carbon monoxide transfer coefficient (Kco)(rho=-0.45, p=0.033) and positively with eNO (rho=0.50, p=0.012). The proportion of IL-4-producing CD8+ T cells was positively correlated with body mass index (rho=0.42, p=0.023) and Kco (rho=0.47, p=0.026).
  
  
  CONCLUSIONS
  It is suggested that Tc1 cells have a detrimental role and that Tc2 cells have a protective role in disease progression.
authors.affiliation: Department of Respiratory Medicine, Shizuoka General Hospital, and Hamamatsu University School of Medicine, Shizuoka, Japan. tmjkshi@general-hosp.pref.shizuoka.jp
authors.forename: Toshihiro
authors.initials: T
authors.lastname: Shirai
authors.forename: Takafumi
authors.initials: T
authors.lastname: Suda
authors.forename: Naoki
authors.initials: N
authors.lastname: Inui
authors.forename: Kingo
authors.initials: K
authors.lastname: Chida
mesh_terms: D000368:Aged; D002097:C-Reactive Protein / Q000378:metabolism; D015704:CD4 Antigens / Q000096:biosynthesis; D016827:CD8 Antigens / Q000096:biosynthesis; D002478:Cells, Cultured; D003602:Cytotoxicity, Immunologic; D005260:Female; D006801:Humans; D007371:Interferon-gamma / Q000378:metabolism; D015847:Interleukin-4 / Q000378:metabolism; D008297:Male; D009504:Neutrophils / Q000473:pathology; D029424:Pulmonary Disease, Chronic Obstructive / Q000097:blood / Q000276:immunology* / Q000503:physiopathology; D012129:Respiratory Function Tests; D012907:Smoking; D013183:Sputum / Q000166:cytology; D016176:T-Lymphocyte Subsets / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D013602:T-Lymphocytes, Cytotoxic / Q000276:immunology / Q000378:metabolism* / Q000473:pathology
chemical_list: D015704:CD4 Antigens; D016827:CD8 Antigens; D015847:Interleukin-4; D007371:Interferon-gamma; D002097:C-Reactive Protein