Department of Microbiology and Immunology, Virginia Commonwealth University, Richmond VA, USA.
J Neuroimmunol. 2011 Apr;233(1-2):80-9. doi: 10.1016/j.jneuroim.2010.11.014. Epub 2011 Jan 6.
CD23 is implicated as a regulator of IgE synthesis. A soluble form of CD23 (sCD23) is released following cleavage by ADAM10 and enhanced sCD23 is correlated with increased IgE. In the CNS, signaling through the kainate receptor (KAR) increases ADAM10. In B cells, activation of KARs produced a significant increase in ADAM10 and sCD23 release as well as an increase in B cell proliferation and immunoglobulin production. In addition, ADAM10 inhibitors reduce IgE synthesis from in vitro cultures of human B cells. Thus, we report for the first time the unique presence of the kainate receptor in B cells and that activation of KARs could serve as a novel mechanism for enhancing B cell activation.
CD23 被认为是 IgE 合成的调节剂。CD23 的一种可溶性形式（sCD23）在被 ADAM10 切割后释放，并且增强的 sCD23 与增加的 IgE 相关。在中枢神经系统中，通过 kainate 受体 (KAR) 的信号传导增加了 ADAM10。在 B 细胞中，KAR 的激活导致 ADAM10 和 sCD23 释放的显著增加，以及 B 细胞增殖和免疫球蛋白产生的增加。此外，ADAM10 抑制剂减少了来自体外培养的人 B 细胞的 IgE 合成。因此，我们首次报道了 kainate 受体在 B 细胞中的独特存在，并且 KAR 的激活可以作为增强 B 细胞激活的新机制。
