Epstein-Barr virus-immortalized B cells produce IL-6 as an autocrine growth factor.
Epstein-Barr virus-immortalized B cells produce IL-6 as an autocrine growth factor.
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Epstein-Barr 病毒永生化 B 细胞产生 IL-6 作为自分泌生长因子。
作者：
T. Yokoi;T. Miyawaki;Akihiro Yachie;K. Kato;Y. Kasahara;N. Taniguchi
EB病毒（EBV）永生化B细胞的持续增殖是由自分泌以及旁分泌生长因子增强。在本研究中，EB病毒永生化B细胞可能产生白细胞介素-6（IL-6）蛋白的自分泌方式的可能性进行了检查。发现来自EBV转化的B细胞而不是来自伯基特淋巴瘤系的培养物上清液增强IL-6依赖性鼠杂交瘤克隆MH60.BSF2的增殖。在EBV转化的B细胞的培养上清液中发现的这种对杂交瘤细胞的生长促进活性被兔抗重组（r）IL-6抗体特异性中和。EB病毒转化的B细胞的培养上清液中的IL-6活性，虽然远低于脂多糖（LPS）刺激的单核细胞，增加了佛波醇肉豆蔻酸酯乙酸酯。使用兔抗rIL-6抗血清的Western印迹实验表明，来自培养的EBV转化的B细胞的上清液含有不同形式的IL-6，峰为23，000 MW。当通过原位杂交分析检查时，发现IL-6 mRNA在EBV转化的B细胞上表达。值得注意的是，这些细胞中的一部分，但不是全部，强烈表达IL-6 mRNA，这意味着它们的细胞周期依赖性表达。此外，显示rIL-6在低细胞密度下促进EBV转化的B细胞的生长。结果表明IL-6在EBV转化的B细胞中起自分泌生长因子的作用。
The continuous proliferation of Epstein-Barr virus (EBV)-immortalized B cells is enhanced by autocrine as well as paracrine growth factors. In the present study, the possibility that EBV-immortalized B cells might produce interleukin-6 (IL-6) proteins in an autocrine manner was examined. It was found that culture supernatants from EBV-transformed B cells, but not from Burkitt's lymphoma lines, augmented the proliferation of an IL-6-dependent murine hybridoma clone, MH60.BSF2. This growth-promoting activity for hybridoma cells found in culture supernatants of EBV-transformed B cells was specifically neutralized by rabbit anti-recombinant (r) IL-6 antibody. The IL-6 activity in culture supernatants of EBV-transformed B cells, though much less than that of lipopolysaccharide (LPS)-stimulated monocytes, was increased by the addition of phorbol myristate acetate. Western blot experiments using rabbit anti-rIL-6 antiserum demonstrated that supernatants from cultured EBV-transformed B cells contained the distinct forms of IL-6, with a peak of 23,000 MW. When examined by in situ hybridization analysis, it was found that IL-6 mRNA were expressed on EBV-transformed B cells. It was noted that a fraction, but not all, of these cells expressed IL-6 mRNA strongly, implying their cell cycle-dependent expression. In addition, it was shown that rIL-6 promoted the growth of EBV-transformed B cells at low cell densities. The results suggest that IL-6 serves as an autocrine growth factor in EBV-transformed B cells.