IL-12 as Well as IL-2 Upregulates CCR5 Expression on T Cell Receptor-Triggered Human CD4+ and CD8+ T Cells
IL-12 as Well as IL-2 Upregulates CCR5 Expression on T Cell Receptor-Triggered Human CD4+ and CD8+ T Cells
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IL-12 和 IL-2 上调 T 细胞受体触发的人 CD4 和 CD8 T 细胞上的 CCR5 表达
DOI：
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发表时间：
2001
影响因子：
9.1
通讯作者：
T. Hamaoka
中科院分区：
文献类型：
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作者：
Yi;M. Tomura;M. Iwasaki;T. Mukai;P. Gao;S. Ono;J. Zou;G. Shearer;H. Fujiwara;T. Hamaoka
白细胞表面趋化因子受体的表达与其活化状态有关。然而，每个趋化因子受体诱导的确切机制知之甚少。在这里，我们研究了CCR 5，一种与T细胞运输和HIV感染有关的趋化因子受体，是如何在人类T细胞中诱导的。在新鲜制备的人外周血单个核细胞（PBMC）群体中少量检测到CCR 5。用IL-2长期（8天）刺激PBMC导致T细胞上高水平的CCR 5表达。IL-12不能在这种直接刺激的PBMC群体中诱导T细胞上的CCR 5。用抗-CD 3加抗-CD 28刺激PBMC T细胞诱导可检测的尽管非常低水平的CCR 5沿着IL-12受体的诱导。然而，当用IL-12刺激时，这些TCR触发的T细胞表达更高水平的CCR 5。虽然IL-2也诱导CCR 5表达，但CCR 5表达在IL-12中比IL-2刺激更有效。这些结果表明，除了IL-2之外，IL-12在诱导T细胞，特别是TCR触发的T细胞上的CCR 5表达中起重要作用。
The expression of chemokine receptors on leukocytes is related to their activation state. However, the exact mechanism underlying the induction of each chemokine receptor is poorly understood. Here, we investigated how CCR5, a chemokine receptor implicated in T cell trafficking and HIV infection, is induced in human T cells. CCR5 was marginally detected on a freshly prepared human peripheral blood mononuclear cell (PBMC) population. Long-term (8-day) stimulation of PBMC with IL-2 resulted in high levels of CCR5 expression on T cells. IL-12 failed to induce CCR5 on T cells in such a directly stimulated PBMC population. Stimulation of PBMC T cells with anti-CD3 plus anti-CD28 induced detectable albeit very low levels of CCR5 along with the induction of IL-12 receptor. However, these TCR-triggered T cells expressed much higher levels of CCR5 when stimulated with IL-12. Although IL-2 also induced CCR5 expression, CCR5 expression was more potent in IL-12 than IL-2 stimulation. These results indicate that, in addition to IL-2, IL-12 plays an important role in the induction of CCR5 expression on T cells, particularly TCR-triggered T cells.
DOI：
10.1073/pnas.94.5.1925
发表时间：
1997-03-04
影响因子：
11.1
作者：
Bleul, CC;Wu, LJ;Mackay, CR
通讯作者：
Mackay, CR