Fischer A, König W
Institut für Medizinische Mikrobiologie und Immunologie, Ruhr-Universität Bochum, FRG.
Immunology. 1990 Dec;71(4):473-9.
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.
有证据表明,糖皮质激素能够调节外周血淋巴细胞(PBL)的CD23表达及可溶性(s)CD23释放。我们证明,白细胞介素-2(IL-2)和IL-4诱导的CD23表达对糖皮质激素的敏感性不同。泼尼松龙抑制健康供体PBL上的自发及IL-2诱导的CD23表达。泼尼松龙对IL-4诱导的CD23表达影响较小,但表达动力学发生改变。表达动力学的调节似乎是由于泼尼松龙的启动作用。研究健康和特应性供体的PBL对泼尼松龙对IL-4诱导的CD23表达的影响的敏感性时,差异也很明显。用金黄色葡萄球菌考恩I株预激活PBL消除了差异。泼尼松龙还抑制未刺激及IL-2或IL-4刺激的PBL的sCD23释放,并增强PBL的免疫球蛋白(E、G、A、M)合成。这种增强似乎是由于启动作用,因为用泼尼松龙预刺激PBL足以增强免疫球蛋白合成。糖皮质激素协同增强有或无自发体外IgE合成的PBL的IL-4诱导的IgE合成。