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正常人B细胞中IgE合成的诱导。同种异体反应性T细胞克隆激活及IgE增强因子激活的序列要求。

Induction of IgE synthesis in normal human B cells. Sequential requirements for activation by an alloreactive T cell clone and IgE-potentiating factors.

作者信息

Leung D Y, Young M C, Wood N, Geha R S

出版信息

J Exp Med. 1986 Mar 1;163(3):713-23. doi: 10.1084/jem.163.3.713.

Abstract

Two human alloreactive T cell clones were established from a one-way mixed lymphocyte culture involving two nonatopic donors, and were assessed for their capacity to induce IgE synthesis by B cells obtained from the original stimulator. The two alloreactive T cell clones studied induced IgG but not IgE synthesis in normal B cells. However, one of the two clones, clone 2H6, induced IgE synthesis in the presence of supernatants from T cell lines derived from patients with the hyper-IgE syndrome (HIE), and enriched for T cells bearing receptors for IgE. These supernatants by themselves caused no IgE synthesis in nonatopic B cells. The potentiating factors in these supernatants were shown to bind to IgE. Time sequence experiments indicated that interaction of the B cells with the alloreactive clone 2H6 renders them responsive to the action of the IgE-potentiating factors. These results indicate that induction of IgE synthesis in normal B cells involves at least two sequential T cell derived signals. Furthermore, T cell clones are heterogenous in their capacity to provide these signals.

摘要

从涉及两名非特应性供体的单向混合淋巴细胞培养物中建立了两个人类同种异体反应性T细胞克隆,并评估了它们诱导从原始刺激细胞获得的B细胞合成IgE的能力。所研究的两个同种异体反应性T细胞克隆在正常B细胞中诱导了IgG合成,但未诱导IgE合成。然而,两个克隆之一,即克隆2H6,在存在来自高IgE综合征(HIE)患者的T细胞系上清液的情况下诱导了IgE合成,这些T细胞系富含带有IgE受体的T细胞。这些上清液本身在非特应性B细胞中不会引起IgE合成。已证明这些上清液中的增强因子与IgE结合。时间序列实验表明,B细胞与同种异体反应性克隆2H6的相互作用使它们对IgE增强因子的作用产生反应。这些结果表明,正常B细胞中IgE合成的诱导至少涉及两个连续的T细胞衍生信号。此外,T细胞克隆在提供这些信号的能力上是异质的。

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