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ORAI 介导的 T 细胞增殖、凋亡和耐受中的钙内流。

ORAI-mediated calcium influx in T cell proliferation, apoptosis and tolerance.

机构信息

Department of Biophysics, University of the Saarland, Gebäude 58, D-66421 Homburg/Saar, Germany.

出版信息

Cell Calcium. 2011 Sep;50(3):261-9. doi: 10.1016/j.ceca.2011.05.015. Epub 2011 Jun 12.

DOI:10.1016/j.ceca.2011.05.015
PMID:21665274
Abstract

Ca(2+) homeostasis controls a diversity of cellular processes including proliferation and apoptosis. A very important aspect of Ca(2+) signaling is how different Ca(2+) signals are translated into specific cell functions. In T cells, Ca(2+) signals are induced following the recognition of antigen by the T cell receptor and depend mainly on Ca(2+) influx through store-operated CRAC channels, which are mediated by ORAI proteins following their activation by STIM proteins. The complete absence of Ca(2+) influx caused by mutations in Stim1 and Orai1 leads to severe immunodeficiency. Here we summarize how Ca(2+) signals are tuned to regulate important T cell functions as proliferation, apoptosis and tolerance, the latter one being a special state of immune cells in which they can no longer respond properly to an otherwise activating stimulus. Perturbations of Ca(2+) signaling may be linked to immune suppressive diseases and autoimmune diseases.

摘要

钙离子稳态控制着多种细胞过程,包括增殖和凋亡。钙离子信号转导的一个非常重要的方面是如何将不同的钙离子信号转化为特定的细胞功能。在 T 细胞中,T 细胞受体识别抗原后会诱导钙离子信号,主要依赖于通过储存操作的 CRAC 通道的钙离子内流,该通道由 STIM 蛋白激活 ORAI 蛋白后介导。Stim1 和 Orai1 突变导致的钙离子内流完全缺失会导致严重的免疫缺陷。在这里,我们总结了钙离子信号如何被调节以调节重要的 T 细胞功能,如增殖、凋亡和耐受,后者是免疫细胞的一种特殊状态,在这种状态下,它们不能再对原本激活的刺激做出适当的反应。钙离子信号转导的紊乱可能与免疫抑制性疾病和自身免疫性疾病有关。

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