Rasul Eahsan, Salamon Daniel, Nagy Noemi, Leveau Benjamin, Banati Ferenc, Szenthe Kalman, Koroknai Anita, Minarovits Janos, Klein George, Klein Eva
Department of Microbiology, Tumor and Cell Biology (MTC), Karolinska Instititet, Stockholm, Sweden.
RT-Europe Nonprofit Research Ltd, Mosonmagyaróvár, Hungary.
PLoS One. 2014 Aug 27;9(8):e106008. doi: 10.1371/journal.pone.0106008. eCollection 2014.
The EBV carrying lines MEC1 and MEC2 were established earlier from explants of blood derived cells of a chronic lymphocytic leukemia (CLL) patient at different stages of progression to prolymphocytoid transformation (PLL). This pair of lines is unique in several respects. Their common clonal origin was proven by the rearrangement of the immunoglobulin genes. The cells were driven to proliferation in vitro by the same indigenous EBV strain. They are phenotypically different and represent subsequent subclones emerging in the CLL population. Furthermore they reflect the clinical progression of the disease. We emphasize that the support for the expression of the EBV encoded growth program is an important differentiation marker of the CLL cells of origin that was shared by the two subclones. It can be surmised that proliferation of EBV carrying cells in vitro, but not in vivo, reflects the efficient surveillance that functions even in the severe leukemic condition. The MEC1 line arose before the aggressive clinical stage from an EBV carrying cell within the subclone that was in the early prolymphocytic transformation stage while the MEC2 line originated one year later, from the subsequent subclone with overt PLL characteristics. At this time the disease was disseminated and the blood lymphocyte count was considerably elevated. The EBV induced proliferation of the MEC cells belonging to the subclones with markers of PLL agrees with earlier reports in which cells of PLL disease were infected in vitro and immortalized to LCL. They prove also that the expression of EBV encoded set of proteins can be determined at the event of infection. This pair of lines is particularly important as they provide in vitro cells that represent the subclonal evolution of the CLL disease. Furthermore, the phenotype of the MEC1 cells shares several characteristics of ex vivo CLL cells.
EBV携带细胞系MEC1和MEC2是早期从一名慢性淋巴细胞白血病(CLL)患者处于向幼淋巴细胞转化(PLL)不同进展阶段的血液来源细胞外植体中建立的。这一对细胞系在几个方面具有独特性。它们共同的克隆起源通过免疫球蛋白基因重排得以证实。这些细胞在体外由同一株内源性EBV驱动增殖。它们在表型上不同,代表了CLL群体中出现的后续亚克隆。此外,它们反映了疾病的临床进展。我们强调,对EBV编码生长程序表达的支持是两个亚克隆共有的起源CLL细胞的重要分化标志物。可以推测,携带EBV的细胞在体外而非体内的增殖反映了即使在严重白血病状态下仍起作用的有效监测。MEC1细胞系在侵袭性临床阶段之前,从处于早期幼淋巴细胞转化阶段的亚克隆中的一个携带EBV的细胞产生,而MEC2细胞系在一年后从具有明显PLL特征的后续亚克隆产生。此时疾病已播散,血液淋巴细胞计数显著升高。EBV诱导具有PLL标志物的亚克隆的MEC细胞增殖,这与早期报道一致,即在早期报道中PLL疾病的细胞在体外被感染并永生化形成LCL。它们还证明在感染时可以确定EBV编码的一组蛋白质的表达。这一对细胞系特别重要,因为它们提供了代表CLL疾病亚克隆进化的体外细胞。此外,MEC1细胞的表型与体外CLL细胞具有几个共同特征。