B-lymphocyte calcium influx.
B-lymphocyte calcium influx.
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DOI：
10.1111/j.1600-065x.2009.00822.x
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发表时间：
2009-09
影响因子：
8.7
通讯作者：
Freedman BD
中科院分区：
文献类型：
--
作者：
King LB;Freedman BD
细胞内钙离子浓度的动态变化决定了淋巴细胞的免疫命运和功能。在过去的几年里，关于淋巴细胞库操作的钙内流机制的重要细节已经被揭示，包括钙释放激活(CRAC)通道的分子识别和负责STORE耗尽后CRAC通道激活的内质网钙传感器(STIM1)。然而，炎症环境中生理刺激后可能对淋巴细胞施加CRAC通道激活的潜在精细调控的细节尚未完全解决。在这篇综述中，我们讨论了B淋巴细胞中存储操作(CRAC介导)和存储非依赖的钙信号的几个未被研究的方面。首先，我们讨论了启动CRAC通道激活对抗原-受体连接通路的潜在新需求。第二，我们将讨论的结果表明，商店和CRAC通道之间的耦合可能受到调节，允许分级激活，以响应ER商店的部分耗尽。第三，我们将讨论通过CRAC通道维持钙内流持续时间的机制。最后，我们讨论了在B细胞中被天然刺激激活的不同的钙离子非选择性阳离子通道(NSCCs)，这些天然钙信号通路和CRAC通道相互交叉调节的可能途径，以及天然钙信号的机制基础和生理后果。
Dynamic changes in cytoplasmic calcium concentration dictate the immunological fate and functions of lymphocytes. During the past few years important details have been revealed about the mechanism of store-operated calcium entry in lymphocytes, including the molecular identity of calcium-release activated (CRAC) channels and the ER calcium sensor (STIM1) responsible for CRAC channel activation following calcium depletion of stores. However, details of the potential fine regulation of CRAC channel activation that may be imposed on lymphocytes following physiologic stimulation within an inflammatory environment have not been fully addressed. In this review, we discuss several underexplored aspects of store-operated (CRAC-mediated) and store-independent calcium signaling in B lymphocytes. First, we discuss the potential novel requirement for antigen-receptor linked pathways in initiating CRAC channel activation. Second, we will discuss results suggesting that coupling between stores and CRAC channels may be regulated, allowing for graded activation in response to partial depletion of ER stores. Third, we will discuss mechanisms that sustain the duration of calcium entry via CRAC channels. Finally, we discuss distinct calcium permeant non-selective cation channels (NSCCs) that are activated by innate stimuli in B cells, potential means by which these innate calcium signaling pathways and CRAC channels crossregulate one another and the mechanistic basis and physiologic consequences of innate calcium signaling.