Lu Y Y, Koga Y, Tanaka K, Sasaki M, Kimura G, Nomoto K
Department of Immunology, Kyushu University, Fukuoka, Japan.
J Virol. 1994 Jan;68(1):390-9. doi: 10.1128/JVI.68.1.390-399.1994.
In a previous study (Y. Koga, M. Sasaki, H. Yoshida, H. Wigzell, G. Kimura, and K. Nomoto, J. Immunol. 144:94-102, 1990), we demonstrated that the expression of gp160, a precursor form of envelope glycoprotein of human immunodeficiency virus type 1, in CD4+ cells causes the downregulation of surface CD4 and single-cell killing by forming intracellular gp160-CD4 complex. In the present study we investigated the events that lead to cell death in CD4+ cells expressing gp160. We found that apoptosis is induced in cells undergoing single-cell death. Moreover, even the cell clone, which expresses so little gp160 that it does not exhibit any apparent cytopathic effects, such as the inhibition of cell growth, was found to be highly susceptible to the apoptosis induction by the anti-Fas monoclonal antibody.
在之前的一项研究中（Y. 古贺、M. 佐佐木、H. 吉田、H. 维格泽尔、G. 木村和K. 野本，《免疫学杂志》144:94 - 102，1990），我们证明了人类免疫缺陷病毒1型包膜糖蛋白前体形式gp160在CD4 + 细胞中的表达会通过形成细胞内gp160 - CD4复合物导致表面CD4下调和单细胞杀伤。在本研究中，我们调查了在表达gp160的CD4 + 细胞中导致细胞死亡的事件。我们发现，正在经历单细胞死亡的细胞会诱导凋亡。此外，即使是表达极少gp160以至于未表现出任何明显细胞病变效应（如细胞生长抑制）的细胞克隆，也被发现对抗Fas单克隆抗体诱导的凋亡高度敏感。
Zotero 插件
