title: Invariant natural killer T cells in asthma and chronic obstructive pulmonary disease.
abstract: BACKGROUND
  The number of type 2 helper CD4+ T cells is increased in the airways of persons with asthma. Whether the majority of these cells are class II major-histocompatibility-complex-restricted cells or are among the recently identified CD1d-restricted invariant natural killer T cells is a matter of controversy. We studied the frequency of invariant natural killer T cells in the airways of subjects with mild or moderately severe asthma to investigate the possibility of an association between the number of invariant natural killer T cells in the airway and disease severity. We also studied whether an increased number of these cells is a feature of chronic obstructive pulmonary disease (COPD).
  
  
  METHODS
  We enumerated invariant natural killer T cells by flow cytometry with the use of CD1d tetramers loaded with alpha-galactosylceramide and antibodies specific to the invariant natural killer T-cell receptor in samples of bronchoalveolar-lavage fluid, induced sputum, and bronchial-biopsy specimens obtained from subjects with mild or moderately severe asthma, subjects with COPD, and healthy control subjects. Real-time polymerase-chain-reaction analysis was performed on bronchoalveolar-lavage cells for evidence of gene expression of the invariant natural killer T-cell receptor.
  
  
  RESULTS
  Fewer than 2% of the T cells obtained from all subjects on airway biopsy, bronchoalveolar lavage, and sputum induction were invariant natural killer T cells, with no significant differences among the three groups of subjects. No expression of messenger RNA for the invariant natural killer T-cell-receptor domains Valpha24 and Vbeta11 was detected in bronchoalveolar-lavage cells from subjects with asthma.
  
  
  CONCLUSIONS
  Invariant natural killer T cells are found in low numbers in the airways of subjects with asthma, subjects with COPD, and controls.
authors.affiliation: Division of Infection, Inflammation, and Repair, University of Southampton, Southampton General Hospital, Southampton, United Kingdom. vijay@soton.ac.uk
authors.forename: Pandurangan
authors.initials: P
authors.lastname: Vijayanand
authors.forename: Grégory
authors.initials: G
authors.lastname: Seumois
authors.forename: Chris
authors.initials: C
authors.lastname: Pickard
authors.forename: Robert M
authors.initials: RM
authors.lastname: Powell
authors.forename: Gilbert
authors.initials: G
authors.lastname: Angco
authors.forename: David
authors.initials: D
authors.lastname: Sammut
authors.forename: Stephan D
authors.initials: SD
authors.lastname: Gadola
authors.forename: Peter S
authors.initials: PS
authors.lastname: Friedmann
authors.forename: Ratko
authors.initials: R
authors.lastname: Djukanovic
mesh_terms: D001249:Asthma / Q000276:immunology*; D001980:Bronchi / Q000276:immunology*; D001992:Bronchoalveolar Lavage Fluid / Q000276:immunology*; D017252:CD3 Complex; D016022:Case-Control Studies; D005434:Flow Cytometry; D015870:Gene Expression; D006801:Humans; D007694:Killer Cells, Natural / Q000276:immunology; D018655:Lymphocyte Count; D016133:Polymerase Chain Reaction; D029424:Pulmonary Disease, Chronic Obstructive / Q000276:immunology*; D012333:RNA, Messenger / Q000378:metabolism; D011948:Receptors, Antigen, T-Cell / Q000235:genetics / Q000378:metabolism; D017452:Receptors, IgG / Q000235:genetics / Q000378:metabolism; D013183:Sputum / Q000276:immunology*; D013601:T-Lymphocytes / Q000276:immunology; D018418:Th2 Cells
chemical_list: D017252:CD3 Complex; D012333:RNA, Messenger; D011948:Receptors, Antigen, T-Cell; D017452:Receptors, IgG