INTERLEUKIN-4 AND LOW-AFFINITY RECEPTOR FOR IGE ON B-CELLS IN PERIPHERAL-BLOOD OF PATIENTS WITH ATOPIC BRONCHIAL-ASTHMA

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 r esponding to IL-4 by an increased synthesis of IgE is also higher in a topic subjects than in nonatopic subjects. Objective: Important questi ons are whether the elevated IgE in atopic subjects is due to overprod uction 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 rela ted to the development of allergic diseases. Methods: Spontaneous and IL-4-induced CD23 expression on B cells was examined to evaluate the r esponse of B cells to IL-4, and production of IL-4 by concanavalin-A-s timulated peripheral blood mononuclear cells (PBMCs) was measured to e valuate the T-cell function in nonatopic normal subjects, atopic norma l subjects, and patients with symptomatic bronchial asthma. Results: I L-4-induced expression of CD23 on B cells was greater in normal atopic subjects and atopic patients with bronchial asthma than in normal non atopic subjects. IL-4 generated by concanavalin A-stimulated PBMCs was also higher in normal atopic subjects and atopic patients with bronch ial 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 e nhanced in atopic subjects. However, neither enhanced B-cell nor T-cel l function is a hallmark in development of allergic diseases.