The actin cytoskeleton coordinates the signal transduction and antigen processing functions of the B cell antigen receptor.

The actin cytoskeleton coordinates the signal transduction and antigen processing functions of the B cell antigen receptor.
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DOI:
10.1007/s11515-013-1272-0
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发表时间:
2013-10
期刊:
Frontiers in biology
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其他
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B细胞抗原受体(BCR)是B细胞表面的传感器,它探测我们体内的外来分子(抗原),并在遇到同种抗原时激活B细胞产生抗体反应。抗原与BCR的结合在细胞质中诱导信号级联,为B细胞的激活提供第一信号。随后,BCR将抗原内化并靶向结合到内体,在内体中抗原被加工成T细胞可识别的形式。辅助性T细胞与B细胞呈递的抗原结合后产生第二激活信号。B细胞的最佳激活需要两种信号,因此依赖于BCR信号和抗原运输功能的协调。与bcr结合的抗原还可诱导B细胞皮质肌动蛋白网络的快速重构。最近的研究表明,这种肌动蛋白重塑是由BCR信号启动和控制的,对BCR的信号和抗原处理功能都是至关重要的,这表明肌动蛋白在协调这两条途径中发挥了作用。在这里,我们将回顾以往和最近关于肌动蛋白在BCR激活和BCR介导的抗原处理过程中的重组的研究,并讨论肌动蛋白重塑如何将BCR信号转化为快速的抗原摄取和处理,同时对BCR信号提供正反馈和负反馈。
The B cell antigen receptor (BCR) is the sensor on the B cell surface that surveys foreign molecules (antigen) in our bodies and activates B cells to generate antibody responses upon encountering cognate antigen. The binding of antigen to the BCR induces signaling cascades in the cytoplasm, which provides the first signal for B cell activation. Subsequently, BCRs internalize and target bound antigen to endosomes, where antigen is processed into T cell recognizable forms. T helper cells generate the second activation signal upon binding to antigen presented by B cells. The optimal activation of B cells requires both signals, thereby depending on the coordination of BCR signaling and antigen transport functions. Antigen binding to the BCR also induces rapid remodeling of the cortical actin network of B cells. While being initiated and controlled by BCR signaling, recent studies reveal that this actin remodeling is critical for both the signaling and antigen processing functions of the BCR, indicating a role for actin in coordinating these two pathways. Here we will review previous and recent studies on actin reorganization during BCR activation and BCR-mediated antigen processing, and discuss how actin remodeling translates BCR signaling into rapid antigen uptake and processing while providing positive and negative feedback to BCR signaling.