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首页> 外文期刊>Pathobiology: journal of immunopathology, molecular and cellular biology >Epstein-Barr virus infection and altered control of apoptotic pathways in posttransplant lymphoproliferative disorders.
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Epstein-Barr virus infection and altered control of apoptotic pathways in posttransplant lymphoproliferative disorders.

机译：EB病毒感染和移植后淋巴增生性疾病中凋亡途径的控制改变。

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Posttransplant lymphoproliferative disorders (PTLD) represent a spectrum of lymphoid diseases complicating the clinical course of transplant recipients. Most PTLD are Epstein-Barr virus (EBV) associated with viral latency type III. Several in vitro studies have revealed an interaction between EBV latency proteins and molecules of the apoptosis pathway. Data on human PTLD regarding an association between Bcl-2 family proteins and EBV are scarce. We analyzed 60 primary PTLD for expression of 8 anti- (Bcl-2, Bcl-XL, and Mcl-1) and proapoptotic proteins (Bak and Bax), the so-called BH3-only proteins (Bad, Bid, Bim, and Puma), as well as the apoptosis effector cleaved PARP by immunohistochemistry. Bim and cleaved PARP were both significantly (p = 0.001 and p = 5.251e-6) downregulated in EBV-positive compared to EBV-negative PTLD [Bim: 6/40 (15%), cleaved PARP: 10/43 (23%), vs. Bim: 13/16 (81%), cleaved PARP: 12/17 (71%)]. Additionally, we observed a tendency toward increased Bcl-2 protein expression (p = 0.24) in EBV-positive PTLD. Hence, we provide evidence of a distinct regulation of Bcl-2 family proteins in EBV-positive versus negative PTLD. The low-expression pattern of the proapoptotic proteins Bim and cleaved PARP together with the high-expression pattern of the antiapoptotic protein Bcl-2 by trend in EBV-positive tumor cells suggests disruption of the apoptotic pathway by EBV in PTLD, promoting survival signals in the host cells.
机译：移植后淋巴增生性疾病（PTLD）代表了一系列淋巴疾病，使移植受体的临床病程复杂化。大多数PTLD是与III型病毒潜伏期有关的爱泼斯坦巴尔病毒（EBV）。几项体外研究表明，EBV潜伏期蛋白与凋亡途径分子之间存在相互作用。关于Bcl-2家族蛋白和EBV之间的关联的人类PTLD数据很少。我们分析了60种主要PTLD中8种抗（Bcl-2，Bcl-XL和Mcl-1）和促凋亡蛋白（Bak和Bax）的表达，即所谓的仅BH3蛋白（Bad，Bid，Bim和Puma）以及凋亡效应因子通过免疫组织化学裂解了PARP。与EBV阴性PTLD相比，EBV阳性的Bim和裂解的PARP均显着下调（p = 0.001和p = 5.251e-6）[Bim：6/40（15％），裂解的PARP：10/43（23％ ），而Bim：13/16（81％），裂解的PARP：12/17（71％）]。此外，我们观察到在EBV阳性PTLD中Bcl-2蛋白表达增加的趋势（p = 0.24）。因此，我们提供了EBV阳性和阴性PTLD中Bcl-2家族蛋白的独特调控证据。 EBV阳性肿瘤细胞趋势中促凋亡蛋白Bim和裂解的PARP的低表达模式以及抗凋亡蛋白Bcl-2的高表达模式表明EBV破坏了PTLD中的凋亡途径，从而促进了PTLD中的生存信号。宿主细胞。

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