Doig D, Chesebro B
J Exp Med. 1979 Jul 1;150(1):10-9. doi: 10.1084/jem.150.1.10.
A single genetic locus, Rfv-3, influenced Friend virus (FV) viremia, loss of FV-induced cell-surface antigens from leukemia cells, and generation of anti-FV antibodies. 30--90 d after FV infection leukemic spleen cells from (B10.A X A)F1 and (B10.A X A.BY)F1 mice (Rfv-3r/s) were found to have low FV-induced cell-surface antigen expression compared to leukemic spleen cells from A and A.BY mice (Rfv-3s/s). In addition, these F1 mice recovered from viremia and generated cytotoxic anti-FV antibodies. A and A.BY mice did not recover from viremia and failed to generate anti-FV antibodies. Anti-FV leukemia cell antibody appeared to mediate FV-antigen loss because decrease of FV cell-surface antigens occurred at the same time as anti-FV antibody appeared in the plasma of F1 mice, and passive transfer of anti-FV antisera induced modulation of FV cell-surface antigens. Rfv-3 did not influence an intrinsic ability of FV antigens to be modulated from Rfv-3s/s leukemia cells because FV antigen loss from Rfv-3s/s spleen cells occurred after transfer of cells to an immune environment.
单一基因座Rfv - 3影响了弗氏病毒(FV)血症、白血病细胞表面FV诱导抗原的丧失以及抗FV抗体的产生。FV感染后30 - 90天,发现(B10.A×A)F1和(B10.A×A.BY)F1小鼠(Rfv - 3r/s)的白血病脾细胞与A和A.BY小鼠(Rfv - 3s/s)的白血病脾细胞相比,FV诱导的细胞表面抗原表达较低。此外,这些F1小鼠从病毒血症中恢复并产生了细胞毒性抗FV抗体。A和A.BY小鼠未从病毒血症中恢复,也未能产生抗FV抗体。抗FV白血病细胞抗体似乎介导了FV抗原的丧失,因为FV细胞表面抗原的减少与抗FV抗体在F1小鼠血浆中出现的时间相同,并且抗FV抗血清的被动转移诱导了FV细胞表面抗原的调节。Rfv - 3不影响FV抗原从Rfv - 3s/s白血病细胞中被调节的内在能力,因为在将Rfv - 3s/s脾细胞转移到免疫环境后,FV抗原才从这些细胞中丧失。