title: Predominant TH2-like bronchoalveolar T-lymphocyte population in atopic asthma.
abstract: BACKGROUND
  In atopic asthma, activated T helper lymphocytes are present in bronchial-biopsy specimens and bronchoalveolar-lavage (BAL) fluid, and their production of cytokines may be important in the pathogenesis of this disorder. Different patterns of cytokine release are characteristic of certain subgroups of T helper cells, termed TH1 and TH2, the former mediating delayed-type hypersensitivity and the latter mediating IgE synthesis and eosinophilia. The pattern of cytokine production in atopic asthma is unknown.
  
  
  METHODS
  We assessed cells obtained by BAL in subjects with mild atopic asthma and in normal control subjects for the expression of messenger RNA (mRNA) for interleukin-2, 3, 4, and 5, granulocyte-macrophage colony-stimulating factor (GM-CSF), and interferon gamma by in situ hybridization with 32P-labeled complementary RNA. Localization of mRNA to BAL T cells was assessed by simultaneous in situ hybridization and immunofluorescence and by in situ hybridization after immunomagnetic enrichment or depletion of T cells.
  
  
  RESULTS
  As compared with the control subjects, the subjects with asthma had more BAL cells per 1000 cell that were positive for mRNA for interleukin-2 (P less than 0.05), 3 (P less than 0.01), 4 (P less than 0.001), and 5 (P less than 0.001) and GM-CSF (P less than 0.001). There was no significant difference between the two groups in the number of cells expressing mRNA for interferon gamma. In the subjects with asthma, mRNA for interleukin-4 and 5 was expressed predominantly by T lymphocytes.
  
  
  CONCLUSIONS
  Atopic asthma is associated with activation in the bronchi of the interleukin-3, 4, and 5 and GM-CSF gene cluster, a pattern compatible with predominant activation of the TH2-like T-cell population.
authors.affiliation: National Heart and Lung Institute, London, United Kingdom.
authors.forename: D S
authors.initials: DS
authors.lastname: Robinson
authors.forename: Q
authors.initials: Q
authors.lastname: Hamid
authors.forename: S
authors.initials: S
authors.lastname: Ying
authors.forename: A
authors.initials: A
authors.lastname: Tsicopoulos
authors.forename: J
authors.initials: J
authors.lastname: Barkans
authors.forename: A M
authors.initials: AM
authors.lastname: Bentley
authors.forename: C
authors.initials: C
authors.lastname: Corrigan
authors.forename: S R
authors.initials: SR
authors.lastname: Durham
authors.forename: A B
authors.initials: AB
authors.lastname: Kay
mesh_terms: D000328:Adult; D000945:Antigens, Differentiation, T-Lymphocyte / Q000032:analysis; D001249:Asthma / Q000276:immunology*; D001992:Bronchoalveolar Lavage Fluid / Q000166:cytology; D017252:CD3 Complex; D002469:Cell Separation; D016207:Cytokines / Q000096:biosynthesis*; D005260:Female; D016178:Granulocyte-Macrophage Colony-Stimulating Factor / Q000096:biosynthesis / Q000235:genetics; D006801:Humans; D007371:Interferon-gamma / Q000096:biosynthesis / Q000235:genetics; D007376:Interleukin-2 / Q000096:biosynthesis / Q000235:genetics; D007377:Interleukin-3 / Q000096:biosynthesis / Q000235:genetics; D015847:Interleukin-4 / Q000096:biosynthesis / Q000235:genetics; D015848:Interleukin-5 / Q000096:biosynthesis / Q000235:genetics; D007958:Leukocyte Count; D008213:Lymphocyte Activation; D008297:Male; D005810:Multigene Family; D009693:Nucleic Acid Hybridization; D012333:RNA, Messenger / Q000032:analysis; D011948:Receptors, Antigen, T-Cell / Q000032:analysis; D006377:T-Lymphocytes, Helper-Inducer / Q000737:chemistry
chemical_list: D000945:Antigens, Differentiation, T-Lymphocyte; D017252:CD3 Complex; D016207:Cytokines; D007376:Interleukin-2; D007377:Interleukin-3; D015848:Interleukin-5; D012333:RNA, Messenger; D011948:Receptors, Antigen, T-Cell; D015847:Interleukin-4; D007371:Interferon-gamma; D016178:Granulocyte-Macrophage Colony-Stimulating Factor