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抗Friend病毒抗体与白血病小鼠病毒血症的恢复及病毒白血病细胞表面抗原的丧失有关。鉴定Rfv-3为影响抗体产生的基因座。

Anti-Friend virus antibody is associated with recovery from viremia and loss of viral leukemia cell-surface antigens in leukemic mice. Identification of Rfv-3 as a gene locus influencing antibody production.

作者信息

Doig D, Chesebro B

出版信息

J Exp Med. 1979 Jul 1;150(1):10-9. doi: 10.1084/jem.150.1.10.

Abstract

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.

摘要

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。

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