Regulation of the expression of IL-6 in human monocytes.
Regulation of the expression of IL-6 in human monocytes.
复制标题
人单核细胞中 IL-6 表达的调节。
作者：
Sébastien Navarro;N. Debili;J. Bernaudin;William Vainchenker;J. Doly
IL-6是具有多种细胞依赖性功能的细胞调节分子。我们已经研究了人单核细胞中IL-6表达的控制，因为它们在这种分子的产生中起关键作用。测试了粘附和不同细胞因子（包括CSF-1、IFN-γ、IL-1 α和粒细胞-巨噬细胞-CSF）对IL-6表达的影响。IL-6 mRNA在PBMC的起始群体中通常不被检测到。粘附诱导单核细胞中IL-6基因表达在不到2小时，随后IL-6分泌。通过粘附引发单核细胞对于CSF-1的IL-6过度诱导更有效。与此相反，高水平的诱导IL-6的IFN-γ在未分级的PBMC不需要坚持和原位杂交显示，IL-6 mRNA存在于单核细胞，但不是在淋巴细胞。对于IL-1 α和粒细胞-巨噬细胞-CSF观察到类似的现象。随后研究了两种细胞系HL-60和U937，其中PMA诱导后发生单核细胞分化。IL-6在这两种细胞系中不能组成型检测，而PMA处理诱导IL-6表达。这种作用在HL-60中是快速的（30分钟）和短暂的，而在U937中诱导72小时后仍能检测到IL-6 mRNA。人rIL-6对U937和HL-60细胞的增殖有抑制作用，并能促进HLA Ⅰ类抗原的表达。
IL-6 is a cellular regulatory molecule with various cell-dependent functions. We have studied the control of IL-6 expression in human monocytes because they play a key role in the production of this molecule. The effects of adherence and different cytokines including CSF-1, IFN-gamma, IL-1 alpha, and granulocyte-macrophage-CSF were tested on IL-6 expression. IL-6 mRNA was usually not detected in the starting population of PBMC. Adherence induced IL-6 gene expression in monocytes in less than 2 h and subsequently IL-6 secretion. Priming of monocytes by adherence was more efficient for IL-6 overinduction by CSF-1. In contrast, high level induction of IL-6 by IFN-gamma in unfractionated PBMC did not require adherence and in situ hybridization revealed that IL-6 mRNA was present in monocytes but not in lymphocytes. A similar phenomenon was observed for IL-1 alpha and granulocyte-macrophage-CSF. Two cell lines, HL-60 and U937, in which monocytic differentiation occurs after induction by PMA, were subsequently investigated. IL-6 was not constitutively detectable in these two cell lines, whereas PMA treatment induced IL-6 expression. This effect was rapid (30 min) and transitory in HL-60, whereas IL-6 mRNA was still detected after 72 h of induction in U937. Addition of human rIL-6 on U937 and HL-60 cells inhibited their proliferation and enhanced expression of HLA class I Ag.