Knöller I, Bujanowski-Weber J, Brings B, König W
Institut für Medizinische Mikrobiologie und Immunologie, Ruhr-Universität Bochum, FRG.
Immunology. 1989 Mar;66(3):368-75.
The influence of IL-2 and IL-4 on the mitogen-induced immunoglobulin E and IgG production in vitro was analysed. Furthermore the expression of Fc epsilon RII (CD23 antigen), as well as the release of its soluble products, the isotype-specific IgE binding factors (IgE-BF), was determined. Recombinant IL-2 (rIL-2) exerted opposite effects on the synthesis of IgE by human lymphocytes that were stimulated either by pokeweed mitogen (PWM) or Staphylococcus aureus Cowan I (SAC). rIL-2 induced a dose-dependent suppression of IgE and IgG synthesis in the presence of PWM. This effect was accompanied by a significant decrease of IgE-binding factor (BF), whereas the expression of Fc epsilon RII was not significantly modulated by rIL-2. A marked increase of IgE production was observed when lymphocytes, prestimulated with SAC for 48 hr, were further incubated with increasing amounts of rIL-2 for 6 days. In contrast, IL-4 in concentrations ranging from 500 to 4.9 U/ml did not lead to an enhancement of IgE synthesis in lymphocytes that were prestimulated with SAC. However, SAC-induced IgG secretion was significantly enhanced by 2.3 U/ml of rIL-4. A dose-dependent enhancement of IgE-BF was observed in SAC-prestimulated lymphocyte cultures in the presence of rIL-2 as well as rIL-4. These results demonstrate that the mitogen used for lymphocyte activation, T-cell-derived lymphokines such as IL-2 and IL-4, and IgE-specific binding factors (soluble CD23), are responsible for the induction of human IgE antibody production in vitro.
分析了白细胞介素-2(IL-2)和白细胞介素-4(IL-4)对丝裂原诱导的体外免疫球蛋白E(IgE)和免疫球蛋白G(IgG)产生的影响。此外,还测定了FcεRII(CD23抗原)的表达及其可溶性产物,即同种型特异性IgE结合因子(IgE-BF)的释放。重组IL-2(rIL-2)对由商陆丝裂原(PWM)或金黄色葡萄球菌Cowan I(SAC)刺激的人淋巴细胞合成IgE产生相反的作用。在PWM存在的情况下,rIL-2诱导IgE和IgG合成呈剂量依赖性抑制。这种作用伴随着IgE结合因子(BF)的显著降低,而rIL-2对FcεRII的表达没有明显调节作用。当用SAC预刺激48小时的淋巴细胞再与增加量的rIL-2孵育6天时,观察到IgE产生显著增加。相反,浓度范围为500至4.9 U/ml的IL-4并未导致用SAC预刺激的淋巴细胞中IgE合成增强。然而,2.3 U/ml的rIL-4显著增强了SAC诱导的IgG分泌。在rIL-2和rIL-4存在的情况下,在SAC预刺激的淋巴细胞培养物中观察到IgE-BF呈剂量依赖性增强。这些结果表明,用于淋巴细胞激活的丝裂原、T细胞衍生的细胞因子如IL-2和IL-4以及IgE特异性结合因子(可溶性CD23)负责体外诱导人IgE抗体产生。