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首页> 外文期刊>Molecular and Cellular Biology >The EBNA2-related resistance towards alpha interferon (IFN-alpha) in Burkitt's lymphoma cells effects induction of IFN-induced genes but not the activation of transcription factor ISGF-3.
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The EBNA2-related resistance towards alpha interferon (IFN-alpha) in Burkitt's lymphoma cells effects induction of IFN-induced genes but not the activation of transcription factor ISGF-3.

机译：伯基特淋巴瘤细胞中与EBNA2相关的对α干扰素（IFN-α）的抗性会诱导IFN诱导的基因的诱导，但不会激活转录因子ISGF-3。

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摘要

Transfection of a plasmid encoding the Epstein-Barr virus (EBV) nuclear antigen 2 (EBNA2) gene confers resistance to the antiproliferative effect of alpha interferon (IFN-alpha) in EBV-negative U968 cells (P. Aman and A. von Gabain, EMBO J. 9:147-152, 1990). We studied the expression of IFN-stimulated genes (ISGs) in two pairs of Burkitt's lymphoma cell lines, differing in the expression of the putative immortalizing gene of EBV, EBNA2. In EBNA2-expressing cells, the induction of four ISGs by IFN-alpha was strongly reduced or, in some cases, abolished. Chloramphenicol acetyltransferase reporter gene constructs containing different IFN-stimulated response elements were transfected into EBNA2-negative and EBNA2-positive cells. Induction of chloramphenicol acetyltransferase activity by IFN was impaired in EBNA2-positive cells. Also, a reporter gene construct driven by an IFN-gamma-sensitive promoter element was affected. However, as revealed by gel shift assays, EBNA2-positive and EBNA2-negative cells exhibited a nearly identical pattern of IFN-stimulated response element-binding proteins. Most important, activation of the factor ISGF-3, which previously has been shown to be required and sufficient for transcriptional activation of IFN-induced genes, was not inhibited in IFN-resistant cells expressing EBNA2. The mechanism of the EBNA2-related IFN resistance seems to be distinct both from the resistance mediated by hepatitis virus and adenovirus gene products and from the IFN resistance in Daudi cell variants. In these three cases, the transcriptional block of IFN-induced genes is due to inhibition of ISGF-3 activation and binding. Our data suggest that the EBNA2-related IFN resistance in Burkitt's lymphoma cells acts downstream of the activation of ISGF-3.
机译：编码爱泼斯坦-巴尔病毒（EBV）核抗原2（EBNA2）基因的质粒的转染赋予了对EBV阴性U968细胞中α干扰素（IFN-α）的抗增殖作用的抗性（P. Aman和A. von Gabain， EMBO J.9：147-152，1990）。我们研究了两对Burkitt淋巴瘤细胞系中IFN刺激基因（ISG）的表达，其在推定的EBV永生基因EBNA2的表达上有所不同。在表达EBNA2的细胞中，IFN-α对4种ISG的诱导被大大降低，或者在某些情况下被废除了。将含有不同IFN刺激的应答元件的氯霉素乙酰基转移酶报告基因构建体转染到EBNA2阴性和EBNA2阳性细胞中。在EBNA2阳性细胞中，IFN诱导的氯霉素乙酰转移酶活性受损。另外，由IFN-γ敏感的启动子元件驱动的报道基因构建体也受到影响。但是，如凝胶位移分析所揭示，EBNA2阳性和EBNA2阴性细胞表现出几乎相同的IFN刺激反应元件结合蛋白模式。最重要的是，以前已证明ISGF-3因子的激活在表达EBNA2的IFN耐药细胞中没有被抑制，而该因子先前已被证明对于IFN诱导基因的转录激活是足够的。 EBNA2相关的IFN耐药机制似乎既不同于肝炎病毒和腺病毒基因产物介导的耐药，也不同于Daudi细胞变体中的IFN耐药。在这三种情况下，IFN诱导基因的转录阻滞是由于抑制了ISGF-3的激活和结合。我们的数据表明，伯基特氏淋巴瘤细胞中EBNA2相关的IFN抵抗在ISGF-3激活的下游起作用。

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