Stimulation of the B cell receptor, CD86 (B7-2), and the β2-adrenergic receptor intrinsically modulates the level of IgG1 and IgE produced per B cell
Stimulation of the B cell receptor, CD86 (B7-2), and the β2-adrenergic receptor intrinsically modulates the level of IgG1 and IgE produced per B cell
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DOI：
10.4049/jimmunol.165.2.680
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发表时间：
2000-07-15
影响因子：
4.4
通讯作者：
Sanders, VM
中科院分区：
文献类型：
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作者：
Kasprowicz, DJ;Kohm, AP;Sanders, VM
我们使用来自野生型、CD 86缺陷型或β 2肾上腺素能受体（β 2 AR）缺陷型小鼠的B细胞的研究结果表明，在每个细胞的基础上，IgG 1和IgE的产生水平可以通过三种机制增加。从未免疫小鼠脾中富集的三硝基苯基特异性B细胞预先暴露于Ag和/或β 2 AR配体特布他林24小时，然后在存在或不存在抗CD 86 Ab的情况下被β 2 AR阴性Th 2细胞克隆或CD 40配体/Sf 9细胞和IL-4活化，数据表明，第一种机制涉及CD 86表达的B细胞受体（BCR）依赖性上调，当CD 86被刺激时，与未刺激的细胞相比，增加产生的IgG 1和IgE的量。第二种机制涉及BCR和β（2）AR依赖性上调CD 86至高于单独刺激任一受体诱导的水平，当CD 86被刺激时，进一步增加产生的IgG 1和IgE的量。第三种机制是BCR非依赖性的，涉及B细胞对IL-4应答能力的β 2 AR依赖性增加。流式细胞术和有限稀释分析表明，IgG 1和IgE的增加与同种型转换事件无关。这些发现表明，BCR、β 2 AR和CD 86参与调节IL-4依赖性IgG 1和IgE的产生。
Our findings using B cells from either wild-type, CD86-deficient, or beta(2)-adrenergic receptor (beta(2)AR)-deficient mice suggest three mechanisms by which the level of IgG1 and IgE production can be increased on a per cell basis. Trinitrophenyl-specific B cells enriched from unimmunized mouse spleens were pre-exposed to Ag and/or the beta(2)AR ligand terbutaline for 24 h before being activated by either a beta(2)AR-negative Th2 cell clone or CD40 ligand/Sf9 cells and IL-4 in the presence or absence of an anti-CD86 Ab, Data suggest that the first mechanism involves a B cell receptor (BCR)-dependent up-regulation of CD86 expression that, when CD86 is stimulated, increases the amount of IgG1 and IgE produced in comparison to unstimulated cells. The second mechanism involves a BCR- and beta(2)AR-dependent up-regulation of CD86 to a level higher than that induced by stimulation of either receptor alone that, when CD86 is stimulated, further increases the amount of IgG1 and IgE produced. The third mechanism is BCR-independent and involves a beta(2)AR-dependent increase in the ability of a B cell to respond to IL-4, Flow cytometric and limiting dilution analyses suggest that the increase in IgG1 and IgE occurs independently from the isotype switching event, These findings suggest that the BCR, the beta(2)AR, and CD86 are involved in regulating IL-4-dependent IgG1 and IgE production.