Vig Monika, Kinet Jean-Pierre
Laboratory of Allergy and Immunology, Department of Pathology, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts 02115, USA.
Nat Immunol. 2009 Jan;10(1):21-7. doi: 10.1038/ni.f.220.
Calcium acts as a second messenger in many cell types, including lymphocytes. Resting lymphocytes maintain a low concentration of Ca2+. However, engagement of antigen receptors induces calcium influx from the extracellular space by several routes. A chief mechanism of Ca2+ entry in lymphocytes is through store-operated calcium (SOC) channels. The identification of two important molecular components of SOC channels, CRACM1 (the pore-forming subunit) and STIM1 (the sensor of stored calcium), has allowed genetic and molecular manipulation of the SOC entry pathway. In this review, we highlight advances in the understanding of Ca2+ signaling in lymphocytes with special emphasis on SOC entry. We also discuss outstanding questions and probable future directions of the field.
钙在包括淋巴细胞在内的多种细胞类型中充当第二信使。静息淋巴细胞维持低浓度的Ca2+。然而,抗原受体的激活通过多种途径诱导细胞外空间的钙内流。淋巴细胞中Ca2+进入的主要机制是通过储存-操作性钙(SOC)通道。SOC通道的两个重要分子成分CRACM1(孔形成亚基)和STIM1(储存钙的传感器)的鉴定,使得对SOC进入途径进行遗传和分子操作成为可能。在本综述中,我们重点介绍了在理解淋巴细胞中Ca2+信号传导方面取得的进展,特别强调了SOC进入。我们还讨论了该领域尚未解决的问题以及可能的未来方向。