Hewitt E L, Ozanne B W, Cushley W
Division of Biochemistry and Molecular Biology, Institute of Biomedical and Life Sciences, University of Glasgow, Glasgow, G12 8QQ, UK.
Cytokine. 1997 Dec;9(12):982-91. doi: 10.1006/cyto.1997.0244.
Studies of the CD25 gene promoter region in T cells have revealed the presence of a 31-bp region, including an 11-bp negative regulatory element (NRE), which profoundly suppresses CD25 expression. This report illustrates that the same region acts as a negative regulator of CD25 expression in human B lymphocytes. Human B cells contain DNA-binding protein activities which bind specifically to an oligonucleotide equivalent to the 11-bp core region of the NRE, and stimulation of tonsillar B cells or Daudi Burkitt's lymphoma B cells with interleukin 4 (IL-4) results in loss of binding activity for oligonucleotides containing the NRE; in contrast, IL-4 enhanced binding activity for the NRE in the Jurkat T cell line. Transient transfection analyses using deletion mutants lacking both the 11-bp core NRE and both the NRE and an adjacent putative retinoic acid response element (RARE) motif illustrated that the NRE element is a functional suppressor of CD25 transcription in B cells. Thus, deletion of the NRE element increased the basal level of CD25 promoter activity and also conferred IL-4 inducibility on reporter gene expression in transiently transfected tonsillar B lymphocytes.
对T细胞中CD25基因启动子区域的研究揭示了一个31bp区域的存在,其中包括一个11bp的负调控元件(NRE),该元件可显著抑制CD25的表达。本报告表明,同一区域在人B淋巴细胞中作为CD25表达的负调控因子发挥作用。人B细胞含有能特异性结合与NRE的11bp核心区域等效的寡核苷酸的DNA结合蛋白活性,用白细胞介素4(IL-4)刺激扁桃体B细胞或Daudi伯基特淋巴瘤B细胞会导致对含NRE的寡核苷酸的结合活性丧失;相反,IL-4增强了Jurkat T细胞系中对NRE的结合活性。使用缺失11bp核心NRE以及同时缺失NRE和相邻假定视黄酸反应元件(RARE)基序的缺失突变体进行的瞬时转染分析表明,NRE元件是B细胞中CD25转录的功能性抑制因子。因此,NRE元件的缺失增加了CD25启动子活性的基础水平,并且还赋予了瞬时转染的扁桃体B淋巴细胞中报告基因表达的IL-4诱导性。