T-cell activation triggers death receptor-6 expression in a NF-κB and NF-AT dependent manner
T-cell activation triggers death receptor-6 expression in a NF-κB and NF-AT dependent manner
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DOI：
10.1016/j.molimm.2011.03.021
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发表时间：
2011-07-01
影响因子：
3.6
通讯作者：
Andera, Ladislav
中科院分区：
文献类型：
--
作者：
Klima, Martin;Brouckova, Adela;Andera, Ladislav
死亡受体 6 (DR6) 显然参与了 T 细胞激活和/或活性的调节，因为其基因破坏导致 CD4+ T 细胞扩增增强、Th2 细胞因子产生，有趣的是，CD4+ T 细胞向炎症部位的迁移也受到损害。然而，免疫系统细胞中 DR6 表达的调节机制尚不完全清楚。在本次通讯中，我们表明 DR6 在人外周血或小鼠淋巴结的静息 T 细胞中不表达，但其表达在 CD3 交联或 PMA/离子霉素激活的 T 淋巴细胞中显着上调。 DR6 表达在活化的人 CD4+ 和 CD8+ T 细胞中短暂增加，并且显然依赖于 NF-κ B 和 NF-AT 信号通路的激活。与原代外周血 T 细胞相反，广泛使用的模型淋巴细胞白血病 T 细胞系 Jurkat 出乎意料地呈 DR6 阳性。 TCR 介导的 Jurkat 细胞刺激通过抑制 DR6 转录而强烈下调 DR6 表达。 (C) 2011 Elsevier Ltd. 保留所有权利。
Death receptor-6 (DR6) apparently participates in the regulation of T-cell activation and/or activity as its genetic disruption results in enhanced CD4+ T-cell expansion, the production of Th2 cytokines, and interestingly also the compromised migration of CD4+ T cells to sites of inflammation. However, the mechanism of regulation of DR6 expression in cells of the immune system is not fully understood. In this communication we show that DR6 is not expressed in resting T cells from human peripheral blood or murine lymph nodes but that its expression is significantly upregulated in CD3 crosslinking or PMA/ionomycin-activated T lymphocytes. DR6 expression is transiently increased in both activated human CD4+ and CD8+ T cells and it is apparently dependent on the activation of NF-kappa B and NF-AT signaling pathways. In contrast to primary peripheral blood T cells, the widely used model lymphoblastic leukemia T-cell line Jurkat is DR6-positive and unexpectedly. TCR-mediated stimulation of Jurkat cells strongly downregulates DR6 expression via suppression of its transcription. (C) 2011 Elsevier Ltd. All rights reserved.