我们前期研究证实: BCR信号能调控肌动蛋白重组,而肌动蛋白重组能够改变BCR的空间结构并提供反馈给BCR信号。CD23作为BCR的共受体，其是否能调控B细胞早期激活事件和肌动蛋白重组尚属未知。此前的研究表明，CD23能够负调控免疫应答但其在记忆性B细胞发育过程中的具体调控机制却是未知。我们近期实验发现记忆性B细胞CD23降低，CD23能参与B细胞早期激活和肌动蛋白的重组。但其中的具体分子机制仍然是未知。本项目拟阐明：CD23调控记忆性B细胞发育, B细胞早期激活和肌动蛋白重组的分子机制。上述问题的研究会让我们更加深入了解CD23调控B细胞活化的具体分子机制。本项目属原创性研究，有助于阐明记忆性B细胞的形成机制，并为疫苗设计和接种方案优化奠定理论基础。

Our previous research has shown that BCR signaling can regulate the actin reorganization, while the actin reorganization can offer feedback to the BCR signaling via modulating the spatiotemporal organization of BCR. CD23 has been considered as the co-receptor of BCR, whether it can regulate the early event of B cell activation and actin reorganization is unknown. Previous researches have indicated CD23 can regulate the primary and secondary immune response, but the detail mechanism of CD23 on the development of memory B cells is unknown. Our recent experiments found that the expression of CD23 was reduced in memory B cells. CD23 can regulate the early event of B cell activation and actin reorganization. But the detail molecular mechanisms underlying these processes are still unknown. In this study, we will investigate the detail mechanism of CD23 to affect the development of memory B cells. Next we will focus on the process that how CD23 regulates the early event of B cell activation. Finally, we are going to study the molecular mechanism of CD23 on actin reorganization. Therefore the above study will further understand the detail molecular mechanism of CD23 on regulating the activation of B cells. The original study of this project will be helpful to clarify the mechanism of memory B cell formation. Furthermore, this study will set the theoretical basis for the vaccine design and optimal vaccination.