Doig D, Chesebro B
J Exp Med. 1978 Nov 1;148(5):1109-21. doi: 10.1084/jem.148.5.1109.
Friend virus (FV)-induced leukemic spleen cells from (B10.A X A)F1 mice were found to lose sensitivity to antibody-mediated lysis during progression of erythroleukemia. This was correlated with a 78% loss of FV-induced cell surface antigens as determined by quantitative absorption of cytotoxic antibodies and with a decreased percentage of leukemic spleen cells showing membrane immunofluorescence with anti-FV antibody. Antigen loss was observed only with virus-induced antigens, and was limited to antigens expressed on the cell surface. FV-induced antigens were regained when low-antigen leukemia cells from late stages of the leukemia were transferred to lethally irradiated nonimmune recipients, but not when these cells were transferred to hyperimmune lethally irradiated recipients. Conversely, when high-antigen leukemic spleen cells from early stages of the erythroleukemia were transferred to hyperimmune irradiated recipients, antigen loss was induced. The immune response to virus-induced antigens appeared to be involved in causing the antigenic changes observed on leukemia cells in this system.
在红白血病进展过程中,发现来自(B10.A×A)F1小鼠的Friend病毒(FV)诱导的白血病脾细胞对抗体介导的裂解失去敏感性。通过细胞毒性抗体的定量吸收测定,这与FV诱导的细胞表面抗原损失78%相关,并且与用抗FV抗体显示膜免疫荧光的白血病脾细胞百分比降低相关。仅在病毒诱导的抗原中观察到抗原丢失,并且仅限于细胞表面表达的抗原。当白血病晚期低抗原白血病细胞转移至致死性照射的非免疫受体时,FV诱导的抗原得以恢复,但转移至超免疫致死性照射受体时则不然。相反,当红白血病早期高抗原白血病脾细胞转移至超免疫照射受体时,会诱导抗原丢失。对病毒诱导抗原的免疫反应似乎参与了该系统中白血病细胞上观察到的抗原变化。