Sherr E H, Stein L D, Dosch H M, Saxon A
J Immunol. 1987 Jun 1;138(11):3836-43.
T cells from highly atopic individuals spontaneously secrete in vitro a factor that specifically induces IgE synthesis from normal human B cells. We investigated the effects of such T cell supernatants derived from atopic individuals (TCSN-A) on functionally distinct B cell subsets to determine at what developmental stage B cells become responsive to this IgE-enhancing activity. B cells from normal and allergic donors were separated into subsets of small resting and large activated cells by density centrifugation or unit gravity sedimentation. When stimulated by TCSN-A, large activated B cells made more IgE than small resting B cells. The difference was as much as 3300% in comparing these subsets from allergic donors. Similarly, resting B cells stimulated by Staphylococcus aureus Cowan I (SAC) made 52 to 125% more IgE in response to TCSN-A than unstimulated small resting B cells. However, IgE production from large B cells, already activated in vivo, was not enhanced by the addition of SAC. Notably, the IgE level synthesized by in vivo large activated B cells from allergic persons was markedly greater than that seen with similar cells from normal donors, whereas resting B cells purified from allergic and normal donors produced comparable levels of IgE in response to TCSN-A. These results suggest that this enhancing activity functions as an IgE differentiation factor for activated B cells. This was further confirmed by the effects of TCSN-A on the IgM- and IgE-secreting EBV-transformed human B cell line K1D5. TCSN-A specifically enhanced IgE synthesis from these cells; TCSN from normal donors, IL 2, IFN-gamma, and BCGF did not. These results confirm that this activity functions as an IgE-specific differentiation factor, directly influencing activated B cells to synthesize IgE.
来自高度特应性个体的T细胞在体外可自发分泌一种因子，该因子能特异性诱导正常人B细胞合成IgE。我们研究了来自特应性个体的此类T细胞上清液（TCSN-A）对功能不同的B细胞亚群的影响，以确定B细胞在什么发育阶段开始对这种IgE增强活性产生反应。通过密度离心或单位重力沉降将正常和过敏供体的B细胞分离为小静止细胞和大活化细胞亚群。当受到TCSN-A刺激时，大活化B细胞比小静止B细胞产生更多的IgE。在比较来自过敏供体的这些亚群时，差异高达3300%。同样，金黄色葡萄球菌Cowan I（SAC）刺激的静止B细胞对TCSN-A的反应产生的IgE比未刺激的小静止B细胞多52%至125%。然而，体内已活化的大B细胞添加SAC后IgE产生并未增强。值得注意的是，过敏个体体内大活化B细胞合成的IgE水平明显高于正常供体的类似细胞，而从过敏和正常供体纯化的静止B细胞对TCSN-A的反应产生的IgE水平相当。这些结果表明，这种增强活性作为活化B细胞的IgE分化因子发挥作用。TCSN-A对分泌IgM和IgE的EB病毒转化的人B细胞系K1D5的影响进一步证实了这一点。TCSN-A特异性增强了这些细胞的IgE合成；来自正常供体的TCSN、IL-2、IFN-γ和BCGF则没有。这些结果证实，这种活性作为一种IgE特异性分化因子发挥作用，直接影响活化B细胞合成IgE。
