Chesebro B, Wehrly K
J Exp Med. 1976 Jan 1;143(1):73-84. doi: 10.1084/jem.143.1.73.
The humoral immune response to Friend virus leukemia was studied in congenic F1 mice differing in their incidence of recovery from leukemia. Antiviral neutralizing antibodies rose in titer in vivo concurrently with disappearance of viremia and fall in spleen virus levels. Cytotoxic antileukemia cell antibodies also appeared at this time. Passive transfer of these antibodies could inactivate low numbers of leukemia cells in vivo; however, mice of both high and low recovery genotypes produced antibodies in equal titer and recovered from viral infection in spite of striking differences in recovery from leukemic splenomegaly. Mice lacking C57BL genes did not produce antibodies or recover from viremia except in rare instances. Recovery from splenomegaly was found to be influenced by three or more C57BL genes independent of the H-2 complex.
在白血病恢复发生率不同的同基因F1小鼠中,研究了对弗瑞德病毒白血病的体液免疫反应。抗病毒中和抗体在体内的滴度随着病毒血症的消失和脾脏病毒水平的下降而同时升高。细胞毒性抗白血病细胞抗体也在此时出现。这些抗体的被动转移可在体内使少量白血病细胞失活;然而,尽管在白血病脾肿大的恢复方面存在显著差异,但高恢复基因型和低恢复基因型的小鼠产生的抗体滴度相同,且都从病毒感染中恢复。缺乏C57BL基因的小鼠除了在罕见情况下外,不产生抗体也不从病毒血症中恢复。发现脾肿大的恢复受三个或更多独立于H-2复合体的C57BL基因影响。