title: Peripheral blood manifestations of T(H)2 lymphocyte activation in stable atopic asthma and during exercise-induced bronchospasm.
abstract: BACKGROUND
  Recently, TH2 lymphocyte activation has been shown to play a key role in initiating and propagating the inflammatory response in asthmatic airways. This is manifest through increased numbers of "activated" CD25-(IL-2R)-bearing T-helper cells and can be seen through the IL-5 driven recruitment of eosinophils and IL-4-mediated B-cell expression of CD23 (low affinity IgE receptor) and ultimately IgE production.
  
  
  OBJECTIVE
  To gain a better understanding of the role of immune cells in asthma by describing the peripheral blood immune cell phenotypes in mild atopic asthma.
  
  
  METHODS
  We enrolled 13 patients with mild atopic asthma and a group of seven nonatopic, nonasthmatic controls. Objective measures of lung function were obtained. The peripheral blood was analyzed by flow cytometry for specific cellular markers at rest and during the development of exercise induced bronchospasm.
  
  
  RESULTS
  At rest the number of CD23-bearing B cells (169/mL versus 117/mL; P = .05) and the number of CD25-bearing T cells (355/mL versus 237/mL; P = .03) were increased in the asthma group. There was a linear relationship between these two lymphocyte subsets and the maximum voluntary ventilation at rest (r = 0.56, P = .01 and r = 0.57, P = .01). With the development of exercise-induced bronchospasm there was a significantly greater increase in CD23-positive B cells (96.7/mL versus 59.7/mL; P = .05) and CD25-positive T cells (111.8/mL versus 45.1; P = .01) in the asthma group.
  
  
  CONCLUSIONS
  These data indicate that TH2 lymphocyte activation is manifested by increased numbers of CD23-bearing B cells and CD25-bearing T cells in the peripheral blood of patients with stable mild atopic asthma. Further, these immune cell subsets correlate with markers of resting lung function and increase in the peripheral blood early after the development of exercise-induced bronchospasm.
authors.affiliation: Maine Medical Center, Portland, USA.
authors.forename: T S
authors.initials: TS
authors.lastname: Hallstrand
authors.forename: K A
authors.initials: KA
authors.lastname: Ault
authors.forename: P W
authors.initials: PW
authors.lastname: Bates
authors.forename: J
authors.initials: J
authors.lastname: Mitchell
authors.forename: R B
authors.initials: RB
authors.lastname: Schoene
mesh_terms: D000328:Adult; D001249:Asthma / Q000276:immunology*; D001402:B-Lymphocytes / Q000276:immunology; D001986:Bronchial Spasm / Q000276:immunology*; D005080:Exercise Test; D006801:Humans; D018799:Intercellular Adhesion Molecule-1 / Q000097:blood; D008213:Lymphocyte Activation; D009000:Monocytes / Q000502:physiology; D017455:Receptors, IgE / Q000032:analysis; D015375:Receptors, Interleukin-2 / Q000032:analysis; D013601:T-Lymphocytes / Q000276:immunology; D018418:Th2 Cells / Q000276:immunology*
chemical_list: D017455:Receptors, IgE; D015375:Receptors, Interleukin-2; D018799:Intercellular Adhesion Molecule-1