INTERLEUKIN-5 ENHANCES INTERLEUKIN 4-INDUCED IGE PRODUCTION BY NORMAL HUMAN B-CELLS - THE ROLE OF SOLUBLE CD23 ANTIGEN
INTERLEUKIN-5 ENHANCES INTERLEUKIN 4-INDUCED IGE PRODUCTION BY NORMAL HUMAN B-CELLS - THE ROLE OF SOLUBLE CD23 ANTIGEN
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DOI：
10.1002/eji.1830180615
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发表时间：
1988-06-01
影响因子：
5.4
通讯作者：
DEVRIES, JE
中科院分区：
文献类型：
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作者：
PENE, J;ROUSSET, F;DEVRIES, JE
白细胞介素4（IL 4）诱导的IgE产生的外周血淋巴细胞和扁桃体细胞从正常供体的IL 5增强剂量依赖性的方式。单独测试的IL 5是无效的。IL 5的协同作用在次优IL 4浓度下最明显，而在饱和IL 4浓度（200-300 U/ml）下，IL 5没有作用。Interferon-.gamma.（IFN-γ）阻断IL 4诱导的IgE合成的抗CD 23抗原的单克隆抗体25的F（ab ″）2片段也在IL 4和IL 5的组合存在下抑制IgE的产生，表明IL 5增强了IL 4诱导IgE产生的活化途径。相反，IL 4（50 U/ml）阻断5-诱导的伊加合成。IL 5在诱导可溶性CD 23（sCD 23）的释放方面无效，但在IL 4存在下，观察到sCD 23的释放增强，前提是IL 4以次优浓度存在。IFN-.gamma.完全阻断IL 4和IL 5诱导的sCD 23释放。这些结果表明，sCD 23释放和IgE合成的诱导之间存在强的定量相关性。从EB病毒转化的B细胞系RPMI 8866中分离的sCD 23在诱导IgE产生方面无效。然而，sCD 23与次优浓度的IL 4协同作用。sCD 23在IL 4饱和浓度下不调节IgE应答。总的来说，这些数据表明sCD 23在由IFN-γ介导的IL 4诱导的IgE合成的调节中起重要的调节作用。和IL 5。
Interleukin 4 [IL 4)-induced IgE production by peripheral blood lymphocytes and tonsil cells from normal donors was enhanced in a dose-dependent fashion by IL5. IL5 tested alone was not effective. The synergistic effects of IL5 were most pronounced at suboptimal IL4 concentrations, whereas at saturating IL4 concentrations (200-300 U/ml), IL5 had no effect. Interferon-.gamma. (IFN-.gamma.) and F(ab'')2 fragments of monoclonal antibody 25 directed against the CD23 antigen, that blocked IL4-induced IgE synthesis, also inhibited the production of IgE in the presence of combinations of IL4 and IL5, indicating that IL5 potentiates the activation pathway through which IL4 induces IgE production. In contrast, IL4 (50 U/ml) blocked 5-induced IgA synthesis. IL5 was ineffective in inducing the release of soluble CD23 (sCD23), but in the presence of IL4 an enhanced release of sCD23 was observed, provided IL4 was present at suboptimal concentrations. IFN-.gamma. completely blocked sCD23 release induced by IL4 and IL5. These results demonstrate that there is a strong quantitative correlation between sCD23 release and induction of IgE synthesis. sCD23 fractionated from the Epstein-Barr virus-transformed B cell line RPMI 8866 was ineffective in inducing IgE production. However, sCD23 acted synergistically with suboptimal concentrations of IL4. sCD23 did not modulate the IgE response at saturating concentrations of IL4. Collectively, these data indicate the sCD23 plays an important regulatory role in the modulation of IL 4-induced IgE synthesis mediated by IFN-.gamma. and IL5.