Lerner R A, Oldstone M B, Cooper N R
Proc Natl Acad Sci U S A. 1971 Oct;68(10):2584-8. doi: 10.1073/pnas.68.10.2584.
The expression of Moloney leukemia virus on the surface of a viral-induced lymphoma cell, availability of the virus to anti-viral antibody, and the nature and extent of activation of the complement system during the cell cycle were studied in vitro. Viral antigen was present on the cell surface, accessible to antibody, and was able to activate complement in the presence of antibody throughout all cellular growth phases, while cytotoxicity was confined to the G(1) phase of cell growth. In addition, when cells were arrested in metaphase, viral antigen could be demonstrated on the cell surface by immunofluorescence, and budding virus was seen by electron microscopy. All nine components of complement were activated on the addition of antibody throughout the cell cycle. Additional experiments indicated that in the presence of antibody, C3 and/or C4 were immunospecifically bound to viral-induced lymphoma cells throughout the cell cycle as a result of complement activation. These results indicate that the inability to lyse the cells in the presence of specific anti-viral antibody and complement during the logarithmic phase of cell growth is not due to the lack of expression of Moloney virus antigen(s) on the cell surface, inaccessibility of this surface antigen(s) to antibody, or failure to activate the complement effector system.
在体外研究了莫洛尼白血病病毒在病毒诱导的淋巴瘤细胞表面的表达、病毒与抗病毒抗体的结合情况以及细胞周期中补体系统激活的性质和程度。病毒抗原存在于细胞表面,可与抗体结合,并在所有细胞生长阶段在抗体存在的情况下激活补体,而细胞毒性则局限于细胞生长的G(1)期。此外,当细胞停滞在中期时,通过免疫荧光可在细胞表面检测到病毒抗原,通过电子显微镜可看到出芽病毒。在整个细胞周期中加入抗体后,补体的所有九个成分均被激活。进一步的实验表明,在抗体存在的情况下,由于补体激活,C3和/或C4在整个细胞周期中均免疫特异性地结合到病毒诱导的淋巴瘤细胞上。这些结果表明,在细胞生长对数期存在特异性抗病毒抗体和补体时无法裂解细胞,并非由于莫洛尼病毒抗原在细胞表面缺乏表达、该表面抗原无法与抗体结合或补体效应系统未被激活。