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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。

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

作者信息

Wendel-Hansen V, Tao W, Ericson M, Klein G, Rosén A

机构信息

Department of Medical Cell Genetics, Karolinska Institutet, Stockholm, Sweden.

出版信息

Int J Cancer. 1992 Feb 20;50(4):589-92. doi: 10.1002/ijc.2910500417.

DOI:10.1002/ijc.2910500417
PMID:1311286
Abstract

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 (cIg) and lytic (EA/VCA) protein expression. Both subpopulations had a similar MHC class-II 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 cIg-positive cells were EBNA-positive in the B6 line compared to 94% in the cIg- 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 cIg.

摘要

基于CD23表达对三株爱泼斯坦-巴尔病毒转化的淋巴母细胞系(LCL)进行分析。比较了EBV-DNA在阳性和阴性亚群中的水平。对其中两株细胞系进一步分析了EBNA、细胞质免疫球蛋白(cIg)和裂解性(EA/VCA)蛋白的表达。两个亚群具有相似的MHC II类转录水平,但CD23阴性亚群的接种效率较低,DNA合成速率也较低。在B6、NAD50和0467.3细胞系中,CD23阴性细胞所含的EBV DNA比相应的CD23阳性群体少2±0.2至6.4±3.0倍。EBNA在81±4.2%至93±3.8%的CD23阳性细胞中表达,而在0至46±8.0%的CD23阴性细胞中表达。B6或NAD50中没有CD23阳性细胞含有任何EA/VCA,而19±2.8%至24±4.2%的CD23阴性细胞对裂解周期相关抗原有阳性反应。在CD23阴性细胞中,70±8.6%至86±6.0%的细胞对细胞质免疫球蛋白呈阳性,而在相应的CD23阳性群体中这一比例为14.7±2.7%至14.9±1.8%。我们之前已经表明,在B6细胞系中,只有18%的cIg阳性细胞为EBNA阳性,而在cIg阴性群体中这一比例为94%。这有两种可能的解释:一部分细胞丢失EBV基因组,随后分化为分泌免疫球蛋白的细胞;或者在分化的、EBV基因组阳性的细胞中EBNA表达下调。我们目前的研究结果支持第一种解释,表明在长期建立的和新转化的LCL中,一定比例的细胞可能会丢失其EBV基因组。这伴随着EBNA阳性细胞百分比的降低、至少一种与病毒诱导的母细胞转化相关的激活标记(CD23)的消失,以及cIg合成的增加。

相似文献

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Cell phenotype (CD23)-dependent variation in EBV genome copy numbers within lymphoblastoid cell lines (LCL).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。
Int J Cancer. 1992 Feb 20;50(4):589-92. doi: 10.1002/ijc.2910500417.
2
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Epstein-Barr virus nuclear protein 2 transactivates a cis-acting CD23 DNA element.爱泼斯坦-巴尔病毒核蛋白2反式激活一个顺式作用的CD23 DNA元件。
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Epstein-Barr virus nuclear antigen 2 specifically induces expression of the B-cell activation antigen CD23.爱泼斯坦-巴尔病毒核抗原2特异性诱导B细胞活化抗原CD23的表达。
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EBV-transformed lymphoblastoid cell lines down-regulate EBNA in parallel with secretory differentiation.EB病毒转化的淋巴母细胞系与分泌性分化同时下调EBNA。
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B cell phenotype-dependent expression of the Epstein-Barr virus nuclear antigens EBNA-2 to EBNA-6: studies with somatic cell hybrids.爱泼斯坦-巴尔病毒核抗原EBNA-2至EBNA-6的B细胞表型依赖性表达:体细胞杂交研究
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Growth inhibition of Epstein-Barr virus-transformed B cells by anti-HLA-DR antibody L243: possible relationship to L243-induced down-regulation of CD23 antigen expression.抗HLA-DR抗体L243对爱泼斯坦-巴尔病毒转化的B细胞的生长抑制作用:与L243诱导的CD23抗原表达下调的可能关系。
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引用本文的文献

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GM-CSF and IL-2 induce specific cellular immunity and provide protection against Epstein-Barr virus lymphoproliferative disorder.粒细胞-巨噬细胞集落刺激因子和白细胞介素-2可诱导特异性细胞免疫,并提供针对爱泼斯坦-巴尔病毒淋巴增殖性疾病的保护作用。
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