Bowen J G, Baldwin R W
Int J Cancer. 1979 Jun 15;23(6):833-9. doi: 10.1002/ijc.2910230615.
It has previously been shown that the tumour-specific antigen of the chemically-induced rat hepatoma D23 has determinants recognised by alloantisera raised against normal syngeneic liver and spleen. However, no reactions were observed with alloantisera raised against syngeneic erythrocytes suggesting that the alloantigeneic determinant responsible for this cross-reactivity is not a major serologically-defined histocompatibility antigen. This concept has been further examined using a defined turkey anti-rat beta 2 microglobulin antiserum. This antiserum failed to block the binding of syngeneic antihepatoma D23 sera to hepatoma D23 target cells as assessed using membrane immunofluorescence and complement-dependant 51Cr release tests. Furthermore, immune precipitates formed from soluble tumour extracts containing hepatoma D23 specific antigen with turkey anti-rat beta 2 microglobulin failed to generate a tumour-specific antibody response in syngeneic rats althouth a cross-reactive antiserum was produced following immunization of allogeneic rats with the immune precipitate.
先前的研究表明,化学诱导的大鼠肝癌D23的肿瘤特异性抗原具有一些决定簇,这些决定簇能被针对同基因正常肝脏和脾脏产生的同种抗血清所识别。然而,用针对同基因红细胞产生的同种抗血清未观察到反应,这表明负责这种交叉反应的同种抗原决定簇不是主要的血清学定义的组织相容性抗原。使用一种明确的火鸡抗大鼠β2微球蛋白抗血清对这一概念进行了进一步研究。使用膜免疫荧光和补体依赖性51Cr释放试验评估,该抗血清未能阻断同基因抗肝癌D23血清与肝癌D23靶细胞的结合。此外,含有肝癌D23特异性抗原的可溶性肿瘤提取物与火鸡抗大鼠β2微球蛋白形成的免疫沉淀物,在同基因大鼠中未能产生肿瘤特异性抗体反应,尽管用该免疫沉淀物免疫异基因大鼠后产生了一种交叉反应抗血清。