Interleukin-4 and low-affinity receptor for IgE on B cells in peripheral blood of patients with atopic bronchial asthma.

Abstract

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. 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. 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. 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. 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.