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将gP85gag鉴定为一种可被在体内发挥作用的莫洛尼白血病病毒特异性细胞溶解T细胞克隆识别的抗原。

Characterization of gP85gag as an antigen recognized by Moloney leukemia virus-specific cytolytic T cell clones that function in vivo.

作者信息

van der Hoorn F A, Lahaye T, Müller V, Ogle M A, Engers H D

出版信息

J Exp Med. 1985 Jul 1;162(1):128-44. doi: 10.1084/jem.162.1.128.

Abstract

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.

摘要

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。

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