title: Sputum T lymphocytes in asthma, COPD and healthy subjects have the phenotype of activated intraepithelial T cells (CD69+ CD103+).
abstract: BACKGROUND
  T cells of intraepithelial phenotype have previously been detected in bronchoalveolar lavage (BAL) fluid in a range of lung diseases; these cells express the adhesion molecule alpha(E)beta(7) integrin, CD103, the ligand for epithelial cell E-cadherin. In subjects with asthma CD4+ lymphocytes are the predominant T cell subtype found in bronchial biopsy specimens and in BAL fluid, whereas CD8+ lymphocytes have been shown to predominate in subjects with chronic obstructive pulmonary disease (COPD). The aim of this study was to analyse the expression of CD103, activation markers (CD25 and CD69), and chemokine receptors (CXCR3, CCR5 and CCR3) on CD4+ and CD8+ lymphocytes from sputum and peripheral blood of subjects with asthma, COPD, and healthy controls.
  
  
  METHODS
  T cell surface markers were assessed by immunofluorescence labelling and flow cytometry of gated lymphocytes among CD45+ leucocytes in sputum cell suspensions.
  
  
  RESULTS
  Sputum lymphocytes expressed higher levels of CD103 and CD69 than blood lymphocytes in all subject groups, with CD103 expressed at higher levels on CD8+ than on CD4+ cells. There were no detectable differences in numbers of CD4+ and CD8+ T cells between subjects with asthma, COPD and controls. The percentage of sputum lymphocytes expressing CXCR3 was lower in subjects with asthma or COPD than in healthy controls; CCR3 was not detectable on sputum or blood lymphocytes.
  
  
  CONCLUSIONS
  Sputum T lymphocytes are predominantly of activated intraepithelial phenotype (CD103+ CD69+), and normal numbers of CD4+ and CD8+ T cell populations are found in the sputum of patients with asthma and COPD.
authors.affiliation: National Heart and Lung Institute (NHLI) Clinical Studies Unit, Imperial College, London, UK.
authors.forename: M J
authors.initials: MJ
authors.lastname: Leckie
authors.forename: G R
authors.initials: GR
authors.lastname: Jenkins
authors.forename: J
authors.initials: J
authors.lastname: Khan
authors.forename: S J
authors.initials: SJ
authors.lastname: Smith
authors.forename: C
authors.initials: C
authors.lastname: Walker
authors.forename: P J
authors.initials: PJ
authors.lastname: Barnes
authors.forename: T T
authors.initials: TT
authors.lastname: Hansel
mesh_terms: D000328:Adult; D015703:Antigens, CD / Q000378:metabolism; D000945:Antigens, Differentiation, T-Lymphocyte / Q000378:metabolism; D000954:Antigens, Surface; D001249:Asthma / Q000276:immunology*; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology; D018414:CD8-Positive T-Lymphocytes / Q000276:immunology; D004229:Dithiothreitol / Q000494:pharmacology; D005260:Female; D005434:Flow Cytometry; D005541:Forced Expiratory Volume / Q000502:physiology; D006801:Humans; D039001:Integrin alpha Chains / Q000378:metabolism; D037181:Lectins, C-Type; D008213:Lymphocyte Activation; D008297:Male; D010641:Phenotype; D029424:Pulmonary Disease, Chronic Obstructive / Q000276:immunology*; D015375:Receptors, Interleukin-2 / Q000276:immunology; D013183:Sputum / Q000166:cytology* / Q000276:immunology; D013601:T-Lymphocytes / Q000276:immunology*; D014797:Vital Capacity / Q000502:physiology; D000099192:CD69 Antigens
chemical_list: D015703:Antigens, CD; D000945:Antigens, Differentiation, T-Lymphocyte; D000954:Antigens, Surface; D004229:Dithiothreitol; D039001:Integrin alpha Chains; D037181:Lectins, C-Type; D015375:Receptors, Interleukin-2; D000099192:CD69 Antigens; C091367:alpha E integrins