Suppr超能文献

白细胞介素-7可增强活化的人T细胞中的白细胞介素-4信使核糖核酸及蛋白质水平。

Interleukin-4 mRNA and protein in activated human T cells are enhanced by interleukin-7.

作者信息

Dokter W H, Sierdsema S J, Esselink M T, Halie M R, Vellenga E

机构信息

Department of Medicine, University of Groningen, The Netherlands.

出版信息

Exp Hematol. 1994 Jan;22(1):74-9.

PMID:8282063
Abstract

We studied the effect of the stroma-derived cytokine interleukin-7 (IL-7) on the expression of IL-4 in human T cells at mRNA and protein level. The results demonstrate that IL-7 did not induce IL-4 mRNA in resting T cells. However, concanavalin A (con A)-induced IL-4 mRNA expression was enhanced by costimulation with con A plus IL-7. Nuclear run-on analysis revealed that IL-7 did not affect the transcription rate of the IL-4 gene. The half-life of con A-induced IL-4 transcripts, however, was increased upon con A plus IL-7 treatment, indicating that the effect of IL-7 is mediated at posttranscriptional level. In accordance with the mRNA results, IL-4 protein was not detected in supernatants of unstimulated T cells or T cells exposed to IL-7. In contrast, IL-7 augmented the con A-induced secretion of IL-4 protein significantly. In addition, it was noticed that anti-IL-1 beta and anti-tumor necrosis factor-alpha (anti-TNF-alpha) did not abolish the effect of IL-7 on the con A-induced IL-4 secretion, indicating that the IL-7 effect is not mediated by the release of these cytokines. These results indicate that a stroma-derived factor can affect IL-4 expression in activated human T cells.

摘要

我们在mRNA和蛋白质水平上研究了基质衍生细胞因子白细胞介素-7(IL-7)对人T细胞中IL-4表达的影响。结果表明,IL-7不会在静息T细胞中诱导IL-4 mRNA表达。然而,伴刀豆球蛋白A(con A)诱导的IL-4 mRNA表达在con A与IL-7共刺激下增强。核转录分析显示,IL-7不影响IL-4基因的转录速率。然而,在con A加IL-7处理后,con A诱导的IL-4转录本的半衰期延长,表明IL-7的作用是在转录后水平介导的。与mRNA结果一致,在未刺激的T细胞或暴露于IL-7的T细胞的上清液中未检测到IL-4蛋白。相反,IL-7显著增强了con A诱导的IL-4蛋白分泌。此外,还注意到抗IL-1β和抗肿瘤坏死因子-α(抗TNF-α)并未消除IL-7对con A诱导的IL-4分泌的作用,表明IL-7的作用不是由这些细胞因子的释放介导的。这些结果表明,一种基质衍生因子可以影响活化的人T细胞中IL-4的表达。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验