van der Hoorn F A, Lahaye T, Müller V, Ogle M A, Engers H D
J Exp Med. 1985 Jul 1;162(1):128-44. doi: 10.1084/jem.162.1.128.
The gag membrane protein gP85gag, encoded by Moloney murine leukemia virus (M-MLV), was identified as a target molecule recognized by Moloney murine sarcoma virus--M-MLV (M-MSV--M-MLV)-specific cytolytic T lymphocyte (CTL) clones. Target cells infected with Ab-X-MLV, an M-MLV-derived mutant virus not encoding gP85gag, were not lysed by the CTL clones. The same CTL clones were shown previously to induce the destruction of M-MLV-induced tumor cells in the peritoneal cavity. We have now characterized CTL-resistant antigen-loss tumor cell variants that have lost the surface antigen, but which retain transcriptionally silent M-MLV genomes. A cloned antigen-loss variant that reverted in vitro to the CTL-susceptible phenotype reexpressed M-MLV genomes that had undergone an insertion event in the region of the viral DNA coding for the gag membrane protein. Intravenous injection of virus-specific CTL clones inhibited tumor formation in mice injected subcutaneously with M-MSV--M-MLV.
莫洛尼氏鼠白血病病毒(M-MLV)编码的gag膜蛋白gP85gag被确定为莫洛尼氏鼠肉瘤病毒-M-MLV(M-MSV-M-MLV)特异性细胞毒性T淋巴细胞(CTL)克隆识别的靶分子。感染了Ab-X-MLV(一种不编码gP85gag的M-MLV衍生突变病毒)的靶细胞未被CTL克隆裂解。先前已证明相同的CTL克隆可诱导腹腔内M-MLV诱导的肿瘤细胞的破坏。我们现在已经鉴定了对CTL耐药的抗原缺失肿瘤细胞变体,这些变体已失去表面抗原,但保留了转录沉默的M-MLV基因组。一个在体外恢复为CTL敏感表型的克隆抗原缺失变体重新表达了M-MLV基因组,该基因组在病毒DNA编码gag膜蛋白的区域发生了插入事件。静脉注射病毒特异性CTL克隆可抑制皮下注射M-MSV-M-MLV的小鼠体内肿瘤的形成。