Suppr超能文献

EB病毒感染可诱导B淋巴细胞中转录因子ATF-2/c-Jun的表达,但在慢性淋巴细胞白血病B细胞中则不然。

EBV infection induces expression of the transcription factors ATF-2/c-Jun in B lymphocytes but not in B-CLL cells.

作者信息

Bandobashi Kentaro, Liu Anquan, Nagy Noémi, Kis Loránd L, Nishikawa Jun, Björkholm Magnus, Klein George, Klein Eva

机构信息

Microbiology and Tumor Biology Center, Karolinska Institute, S-171 77, Stockholm, Sweden.

出版信息

Virus Genes. 2005 May;30(3):323-30. doi: 10.1007/s11262-004-6774-z.

Abstract

B cell type chronic lymphocytic leukaemia (B-CLL) cells carry the Epstein-Barr virus (EBV) receptor CD21 and can be infected in vitro with the virus. The infected cells exhibit an unusual EBV program, they express the nuclear proteins but not latent membrane protein 1 (LMP-1). Similar cells were encountered in lymphoid tissues of infectious mononucleosis (IM) patients and in lymphoproliferations of immunosuppressed patients. EBV infected B-CLL cells can be regarded as model for this viral program. In B cells the regulation of LMP-1 is executed mainly by EBV encoded nuclear antigen 2 (EBNA-2), interacting with several cellular proteins and these complexes bind to specific sequences in the LMP-1 promoter. ATF2 and c-Jun were shown to be among the interacting partners of EBNA-2. These molecules can be detected in experimentally infected B lymphocytes. We found c-Jun and/or phosphorylated ATF-2 (p-ATF-2) expression in some B-CLL ex vivo samples. They disappeared or their expression declined promptly in explanted cells, even if they were infected with EBV in vitro. Activation of the infected B-CLL cells by exposure to CD40L was accompanied by p-ATF-2 and c-Jun but not by LMP-1 expression. In one of three clones tested, subsequent treatment with histone deacetylase inhibitors (HDACi), TSA or n-butyrate, could induce LMP-1. Treatment with phorbol-12, 13-dibutyrate (PDB) induced LMP-1 expression in three of four clones. Neither the HDACi nor the PDB treated cells survived.

摘要

B细胞型慢性淋巴细胞白血病(B-CLL)细胞携带爱泼斯坦-巴尔病毒(EBV)受体CD21,并且在体外可被该病毒感染。被感染的细胞呈现出一种不寻常的EBV程序,它们表达核蛋白但不表达潜伏膜蛋白1(LMP-1)。在传染性单核细胞增多症(IM)患者的淋巴组织以及免疫抑制患者的淋巴增殖中也发现了类似的细胞。EBV感染的B-CLL细胞可被视为这种病毒程序的模型。在B细胞中,LMP-1的调控主要由EBV编码的核抗原2(EBNA-2)执行,EBNA-2与几种细胞蛋白相互作用,这些复合物结合到LMP-1启动子中的特定序列。ATF2和c-Jun被证明是EBNA-2的相互作用伙伴。这些分子可以在实验感染的B淋巴细胞中检测到。我们在一些体外B-CLL样本中发现了c-Jun和/或磷酸化的ATF-2(p-ATF-2)表达。它们在移出的细胞中消失或其表达迅速下降,即使这些细胞在体外被EBV感染。通过暴露于CD40L激活被感染的B-CLL细胞会伴随着p-ATF-2和c-Jun的出现,但不会伴随着LMP-1的表达。在测试的三个克隆中的一个中,随后用组蛋白去乙酰化酶抑制剂(HDACi)、曲古抑菌素A(TSA)或丁酸盐处理,可以诱导LMP-1的表达。用佛波醇-12,13-二丁酸酯(PDB)处理在四个克隆中的三个中诱导了LMP-1的表达。HDACi和PDB处理的细胞均未存活。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验