Purkerson J M, Newberg M, Wise G, Lynch K R, Isakson P C
Department of Pharmacology, University of Virginia Medical School, Charlottesville 22908.
J Exp Med. 1988 Sep 1;168(3):1175-80. doi: 10.1084/jem.168.3.1175.
We have analyzed requirements for IL-4-induced secretion of IgG1 from anti-Ig-activated B cells. Activated B cell blasts prepared by culture of high density B cells with anti-Ig failed to secrete IgG1 upon subsequent culture with LPS and IL-4. However, IL-4 markedly suppressed IgM secretion in the same cultures. Addition of a mixture of T cell-derived lymphokines or rIL-5 to LPS-stimulated anti-Ig blasts restored IL-4-stimulated IgG1 secretion; rIL-2 further enhanced the response to IL-4 + rIL-5. These results suggest that IL-4, IL-5, and IL-2 cooperate in the regulation of B lymphocyte Ig isotype expression.
我们分析了白细胞介素-4(IL-4)诱导抗免疫球蛋白(Ig)激活的B细胞分泌IgG1的条件。用抗Ig培养高密度B细胞制备的活化B细胞母细胞,在随后用脂多糖(LPS)和IL-4培养时未能分泌IgG1。然而,IL-4在相同培养物中显著抑制IgM分泌。向LPS刺激的抗Ig母细胞中添加T细胞衍生的淋巴因子混合物或重组白细胞介素-5(rIL-5)可恢复IL-4刺激的IgG1分泌;重组白细胞介素-2(rIL-2)进一步增强了对IL-4 + rIL-5的反应。这些结果表明,IL-4、IL-5和IL-2在B淋巴细胞Ig同种型表达的调节中协同作用。