title: Interleukin-4 and low-affinity receptor for IgE on B cells in peripheral blood of patients with atopic bronchial asthma.
abstract: BACKGROUND
  A greater frequency of type 2 helper cells producing IL-4 without interferon-gamma is thought to be responsible for the elevated IgE in serum of atopic subjects. However, the proportion of B cells responding to IL-4 by an increased synthesis of IgE is also higher in atopic subjects than in nonatopic subjects.
  
  
  OBJECTIVE
  Important questions are whether the elevated IgE in atopic subjects is due to overproduction of IL-4 by T cells, the enhanced sensitivity of B cells to IL-4, or both and whether functional alterations of T and B cells are related to the development of allergic diseases.
  
  
  METHODS
  Spontaneous and IL-4-induced CD23 expression on B cells was examined to evaluate the response of B cells to IL-4, and production of IL-4 by concanavalin-A-stimulated peripheral blood mononuclear cells (PBMCs) was measured to evaluate the T-cell function in nonatopic normal subjects, atopic normal subjects, and patients with symptomatic bronchial asthma.
  
  
  RESULTS
  IL-4-induced expression of CD23 on B cells was greater in normal atopic subjects and atopic patients with bronchial asthma than in normal nonatopic subjects. IL-4 generated by concanavalin A-stimulated PBMCs was also higher in normal atopic subjects and atopic patients with bronchial asthma than in normal non-atopic subjects. The expression of CD23 on B cells and IL-4 generation by concanavalin-A-stimulated PBMCs were not different between normal atopic subjects and atopic patients with bronchial asthma.
  
  
  CONCLUSIONS
  Both B-cell and T-cell functions are enhanced in atopic subjects. However, neither enhanced B-cell nor T-cell function is a hallmark in development of allergic diseases.
authors.affiliation: Department of Internal Medicine, Soonchunhyang University Hospital, Seoul, Korea.
authors.forename: C S
authors.initials: CS
authors.lastname: Park
authors.forename: D J
authors.initials: DJ
authors.lastname: Ra
authors.forename: S M
authors.initials: SM
authors.lastname: Lee
authors.forename: S W
authors.initials: SW
authors.lastname: Jeong
authors.forename: S
authors.initials: S
authors.lastname: Uh
authors.forename: H T
authors.initials: HT
authors.lastname: Kim
authors.forename: Y H
authors.initials: YH
authors.lastname: Kim
mesh_terms: D000328:Adult; D001249:Asthma / Q000097:blood / Q000276:immunology*; D001402:B-Lymphocytes / Q000378:metabolism*; D004306:Dose-Response Relationship, Immunologic; D005260:Female; D006801:Humans; D007073:Immunoglobulin E / Q000097:blood; D015847:Interleukin-4 / Q000096:biosynthesis / Q000097:blood* / Q000494:pharmacology; D008297:Male; D017455:Receptors, IgE / Q000032:analysis* / Q000096:biosynthesis / Q000737:chemistry; D013601:T-Lymphocytes / Q000378:metabolism
chemical_list: D017455:Receptors, IgE; D015847:Interleukin-4; D007073:Immunoglobulin E