Regulation of CD23 expression, soluble CD23 release and immunoglobulin synthesis of peripheral blood lymphocytes by glucocorticoids

Abstract

Evidence was obtained that glucocorticoids are capable of modulating the CD23 expression and soluble(s) CD23 release of peripheral blood lymphocytes (PBL). We demonstrate that interleukin-2 (IL-2)- and IL-4-induced CD23 expression are susceptible to glucocorticoids to a different degree. Prednisolone suppressed the spontaneous and IL-2-induced CD23 expression on PBL of healthy donors. The IL-4-induced CD23 expression was influenced much less by prednisolone, but the expression kinetics was altered. The modulation of the expression kinetics appears to be due to a priming effect of prednisolone. Differences were also apparent when the susceptibility of PBL from healthy and atopic donors towards the effect of prednisolone on the IL-4-induced CD23 expression was studied. Preactivation of PBL with Staphylococcus aureus strain Cowan I abolished the differences. Prednisolone also suppressed the sCD23 release from unstimulated and IL-2- or IL-4-stimulated PBL and enhanced the immunoglobulin (E,G,A,M) synthesis of PBL. This enhancement appears to be due to a priming effect, since pre-stimulation of PBL with prednisolone was sufficient to enhance the immunoglobulin synthesis. The IL-4-induced IgE synthesis of PBL with or without spontaneous in vitro IgE synthesis was synergistically enhanced by glucocorticoids.