Abstract
BACKGROUND: A greater frequency of type 2 helper cells producing IL-4 without interferon-γ 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. (J A LLERGY C LIN I MMUNOL 1996;97:1121-8.)
Published Version
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