Cell phenotype (CD23)-dependent variation in EBV genome copy numbers within lymphoblastoid cell lines (LCL).

Cell phenotype (CD23)-dependent variation in EBV genome copy numbers within lymphoblastoid cell lines (LCL).
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淋巴母细胞系 (LCL) 内 EBV 基因组拷贝数的细胞表型 (CD23) 依赖性变异。

DOI:
10.1002/ijc.2910500417
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发表时间:
1992
影响因子:
6.4
通讯作者:
Rosén,A
Rosén,A
中科院分区:
医学1区
文献类型:
--
作者:
Wendel-Hansen,V;Tao,W;Ericson,M;Klein,G;Rosén,A

文献摘要

相似文献

基于其CD 23表达,分析了三种Epstein巴尔病毒转化的淋巴母细胞样细胞系(LCL)。在阳性和阴性亚群中比较EBV-DNA水平。进一步分析了两个系的EBNA、胞质免疫球蛋白(clg)和裂解(EA/VCA)蛋白表达。两个亚群具有相似的MHC class-11转录,但CD 23 −亚群具有较低的平板接种效率和较低的DNA合成速率。在B6、NAD 50和0467.3细胞系中,CD 23 −细胞所含的EBV DNA比相应的CD 23+细胞群少2 ± 0.2-6.4 ± 3.0倍。EBNA在81 ± 4.2%-93 ± 3.8%的CD 23+细胞和0-46 ± 8.0%的CD 23 −细胞中表达。B6或NAD 50中的CD 23+细胞不含任何EA/VCA,而19 ± 2.8%-24 ± 4.2%的CD 23 −细胞对溶解周期相关抗原呈阳性。在CD 23 −细胞中,70 ± 8.6%-86 ± 6.0%为胞浆免疫球蛋白阳性,而相应的CD 23+细胞群中为14.7 ± 2.7%-14.9 ± 1.8%。我们之前已经表明,在B6系中只有18%的clg阳性细胞是EBNA阳性的,而在clg群体中为94%。这有两种不同的解释:一部分细胞的EBV基因组丢失,随后分化为分泌性免疫球蛋白产生,或分化中EBV基因组阳性细胞的EBNA表达下调。我们目前的研究结果支持第一种选择,表明在长期建立和新鲜转化的LCL中,一定比例的细胞可能会丢失其EBV基因组。这伴随着EBNA阳性细胞的百分比降低,与病毒诱导的原始细胞转化相关的至少一种活化标志物(CD 23)消失,以及clg合成增加。
Three Epstein‐Barr‐virus‐transformed lymphoblastoid cell lines (LCL) were analysed on the basis of their CD23 expression. Levels of EBV‐DNA were compared in the positive and negative subpopulations. Two lines were further analysed with regard to EBNA, cytoplasmic immunoglobulin (clg) and lytic (EA/VCA) protein expression. Both subpopulations had a similar MHC class‐11 transcription, but the CD23−subpopulation had a lower plating efficiency and a lower rate of DNA synthesis. In the B6, NAD50 and 0467.3 cell lines, CD23−cells contained 2 ± 0.2–6.4 ± 3.0 times less EBV DNA than the corresponding CD23+population. EBNA was expressed in 81 ± 4.2%‐93 ± 3.8% of the CD23+cells and in 0–46 ± 8.0% of the CD23−cells. No CD23+cells in B6 or NAD50 contained any EA/VCA, while 19 ± 2.8%‐24 ± 4.2% of the CD23−cells were positive for the lytic‐cycle‐associated antigens. Of the CD23−cells, 70 ± 8.6%‐86 ± 6.0% were positive for cytoplasmic immunoglobulin compared to 14.7 ± 2.7%‐14.9 ± 1.8% in the corresponding CD23+population. We have previously shown that only 18% of the clg‐positive cells were EBNA‐positive in the B6 line compared to 94% in the clg population. This was open to 2 alternative interpretations: loss of EBV genomes from a fraction of the cells with subsequent differentiation to secretory immunoglobulin production, or down‐regulation of EBNA expression in differentiating, EBV‐genome‐positive cells. Our present findings speak for the first alternative, indicating that a certain proportion of the cells may lose their EBV genomes in both long‐established and freshly transformed LCLs. This is accompanied by a reduced percentage of EBNA‐positive cells, the disappearance of at least one activation marker (CD23) associated with the virally induced blast transformation, and an increased synthesis of clg.