Zinc enhances the expression of interleukin-2 and interleukin-2 receptors in HUT-78 cells by way of NF-KB activation
Zinc enhances the expression of interleukin-2 and interleukin-2 receptors in HUT-78 cells by way of NF-KB activation
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DOI：
10.1067/mlc.2002.127908
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发表时间：
2002-10-01
期刊：
影响因子：
--
通讯作者：
Sarkar, FH
中科院分区：
文献类型：
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作者：
Prasad, AS;Bao, B;Sarkar, FH
锌缺乏的人白细胞介素（IL）-2的产生减少，锌对IL-2介导的T细胞活化至关重要。我们使用人Th-0恶性淋巴母细胞系HUT-78，研究锌对PHA/PMA激活的T细胞产生IL-2的影响。在缺锌细胞中，IL-2的基因表达比锌充足细胞减少50%。锌的作用是特异性的，并在转录水平。我们还显示了锌对IL-2受体α和β基因表达的显著影响。在缺锌细胞中，NF-κ B（一种锌依赖性转录因子）与DNA的结合减少。通过转染反义NF-κ B p105（NF-κ B p50的前体）表达载体，我们发现，IL-2和IL-2 R α基因表达的降低可能部分是由于锌缺乏细胞中NF-κ B活化的降低。我们的研究首次证实了锌在HUT-78细胞中IL-2及其受体基因表达中的作用。我们还记录了NF-κ B与DNA的结合受到不利影响，从而降低了锌缺乏的HUT-78细胞中IL-2和IL-2 Ra的基因表达。
Production of interleukin (IL)-2 is decreased in zinc-deficient human beings, and zinc is essential to IL-2-mediated T-cell activation. We used a human Th-0 malignant lymphoblastoid cell line, HUT-78, to study the effect of zinc on IL-2 production in PHA/PMA activated T-cells. In zinc-deficient cells, the gene expression of IL-2 was decreased by 50% compared with that in zinc-sufficient cells. The effect of zinc was specific and at the transcriptional level. We also showed a significant effect of zinc on the gene expression of IL-2 receptors alpha and beta. Binding of NF-kappaB (a zinc-dependent transcription factor) to DNA was decreased in zinc-deficient cells. Using transfection of expression vectors of anti-sense NF-kappaB p105 (precursor of NF-kappaB p50) in cells, we showed that a decrease in gene expression of IL-2 and IL-2 Ralpha may be partly due to decreased activation of NF-kappaB in zinc-deficient cells. Our studies demonstrate, for the first time, the role of zinc in gene expression of IL-2 and its receptors in HUT-78 cells. We also document that the binding of NF-kappaB to DNA was adversely affected, thereby decreasing the gene expression of IL-2 and IL-2 Ralpha in zinc-deficient HUT-78 cells.