Schmidt W, Leben L, Atfield G, Festenstein H
Immunogenetics. 1981;14(3-4):323-39. doi: 10.1007/BF00342201.
The antigenic profile of the K-GV tumor of BALB.K origin, induced by Gross virus and maintained in vitro and in vivo, was investigated by serological and immunochemical methods and techniques of cell-mediated immunity. The H-2Kk-gene products were absent by several criteria: (1) monoclonal antibody and conventional alloantisera directed against eh H-2Kk antigenic specificities were nonreactive by direct testing and by absorptions. (2) H-2Kk products could not be precipitated from glycoprotein or protein extracts of the radiolabeled K-GV tumor. (3) Cytotoxic effectors against H-2Kk produced by sensitization in vitro and in vivo failed to kill K-GV target cells. (4) The tumor could neither stimulate BALB.B congenic mice to produce cytotoxic effectors nor specific cytotoxic antibody against H-2Kk-gene products. In contrast, the H-2Dk antigen was readily detectable by all these criteria. These findings therefore describe a tumor which has selectively lost the H-2K-gene products. The K-GV tumor was able to generate Gross-virus specific CTL, but had greatly reduced susceptibility to lysis by Gross-virus specific CTL generated by H-2K expressing AKR (H-2k) tumors. These findings have important implications for the associative recognition of tumor antigens and the immune surveillance of virally induced tumors.
用血清学、免疫化学方法及细胞介导免疫技术,对由格罗斯病毒诱导并在体内外维持的BALB.K来源的K-GV肿瘤的抗原特性进行了研究。根据多项标准,H-2Kk基因产物缺失:(1)针对H-2Kk抗原特异性的单克隆抗体和传统同种异体抗血清,通过直接检测和吸收试验均无反应。(2)无法从放射性标记的K-GV肿瘤的糖蛋白或蛋白质提取物中沉淀出H-2Kk产物。(3)在体外和体内致敏产生的针对H-2Kk的细胞毒性效应细胞未能杀死K-GV靶细胞。(4)该肿瘤既不能刺激BALB.B同源基因小鼠产生细胞毒性效应细胞,也不能产生针对H-2Kk基因产物的特异性细胞毒性抗体。相比之下,通过所有这些标准都能很容易地检测到H-2Dk抗原。因此,这些发现描述了一种选择性丢失H-2K基因产物的肿瘤。K-GV肿瘤能够产生格罗斯病毒特异性CTL,但对由表达H-2K的AKR(H-2k)肿瘤产生的格罗斯病毒特异性CTL的裂解敏感性大大降低。这些发现对肿瘤抗原的联合识别以及病毒诱导肿瘤的免疫监视具有重要意义。