Genovesi E V, Marx P A, Wheelock E F
J Exp Med. 1977 Aug 1;146(2):520-34. doi: 10.1084/jem.146.2.520.
Friend leukemia virus (FLV) erythroleukemic cells cultured in medium containing FLV-immune serum from dormant FLV-infected mice undergo modulation of FLV cell surface antigens. Modulation was determined by an increased resistance to FLV antibody-mediated complement-dependent lysis and was associated temporally with the capping of FLV-immune complexes at the cell surface. Modulated cells regained their susceptibility to FLV antibody-mediated complement-dependent lysis when transferred to medium containing normal mouse serum. After 48 h of culture in FLV-immune serum, 26% of the FLV erythroleukemic cells were devoid of FLV cell surface antigens as demonstrated by immunofluoresence. Antigenic modulation occurred to a greater extent in cells maintained in logarithmic growth than in cells in GO or resting phase. FLV-antigenic modulation is discussed as a possible mechanism by which antibody induces and maintains FLV-transformed cells in a dormant state.
在含有来自潜伏感染了Friend白血病病毒(FLV)的小鼠的FLV免疫血清的培养基中培养的FLV红白血病细胞,会发生FLV细胞表面抗原的调节。调节通过对FLV抗体介导的补体依赖性裂解的抗性增加来确定,并且在时间上与细胞表面FLV免疫复合物的帽化相关。当转移到含有正常小鼠血清的培养基中时,被调节的细胞恢复了对FLV抗体介导的补体依赖性裂解的敏感性。在FLV免疫血清中培养48小时后,通过免疫荧光证明,26%的FLV红白血病细胞缺乏FLV细胞表面抗原。与处于G0期或静止期的细胞相比,对数生长期的细胞中抗原调节的程度更大。FLV抗原调节被讨论为抗体诱导并维持FLV转化细胞处于休眠状态的一种可能机制。