首页> 外文期刊>The Journal of Experomental Medicine >Antigenic properties of cultured tumor cell lines derived from spleens of Friend virus-infected BALB/c and BALB/c-H-2b mice.
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Antigenic properties of cultured tumor cell lines derived from spleens of Friend virus-infected BALB/c and BALB/c-H-2b mice.

机译:来源于Friend病毒感染的BALB / c和BALB / c-H-2b小鼠脾脏的培养肿瘤细胞系的抗原特性。

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BALB/c-H-2b (BALB.B) mice are less susceptible to the Friend virus (FV) disease syndrome than congenic BALB/c (H-2d) mice, and spleen cells from FV-infected BALB.B mice are markedly less tumorigenic on transplantation to syngeneic hosts than those from FV-infected BALB/c mice. For these reasons we investigated the expression of FV-associated cell surface antigens on cultured, FV-trnasformed cell lines of BALB.B and BALB/c origin. Both cell lines induced transplantation immunity in syngeneic hosts toward further implantations of the same tumor, BALB.B cells being significantly more potent in this respect than BALB/c cells. BALB.B tumor cells, which produce complete, infectious FV, expressed both the cell surface antigen, FMR (corresponding to the cytotoxic antibodies in anti-FV antisera), and virus envelope antigen (VEA, corresponding to the virus-neutralizing antibodies in the anti-FV antisera). BALB/c tumor cells, on the other hand, which are FV-nonproducers, expressed no FMR antigen, but did express VEA on their surfaces for at least 100 passages in culture. These cells could induce FV-neutralizing but not cytotoxic anti-FMR antibodies when used to immunize syngeneic hosts. The absence of FMR antigen may be the basis for the reduced capacity of BALB/c tumor cells, by comparison with BALB.B tumor cells, to induce transplantation immunity. After about the 125th serial transfer in culture, BALB/c tumor cells spontaneously ceased to express VEA and simultaneously became very weak inducers of transplantation immunity in BALB/c hosts. This loss of VEA did not stem from the loss of either the spleen focus-forming virus or the helper virus genomes from these cells, since both viruses could still be recovered from the cell line.
机译:与同质BALB / c(H-2d)小鼠相比,BALB / cH-2b(BALB.B)小鼠对Friend病毒(FV)疾病综合征的敏感性较低,而FV感染的BALB.B小鼠的脾细胞的致瘤性明显降低感染FV感染的BALB / c小鼠的同种宿主。由于这些原因,我们研究了FV相关的细胞表面抗原在BALB.B和BALB / c来源的培养的,经FV转化的细胞系中的表达。两种细胞系均诱导同种宿主对同一肿瘤的进一步移植产生移植免疫,BALB.B细胞在这方面比BALB / c细胞具有更高的效力。产生完整传染性FV的BALB.B肿瘤细胞表达细胞表面抗原FMR(对应于抗FV抗血清中的细胞毒性抗体)和病毒包膜抗原(VEA,对应于细胞中的病毒中和抗体)抗FV抗血清)。另一方面,非FV产生者的BALB / c肿瘤细胞不表达FMR抗原,但在其表面至少培养100代时确实表达VEA。当用于免疫同基因宿主时,这些细胞可以诱导FV中和,但不能诱导细胞毒性的抗FMR抗体。与BALB.B肿瘤细胞相比,FMR抗原的缺乏可能是BALB / c肿瘤细胞诱导移植免疫能力降低的基础。在培养物中第125次连续转移后,BALB / c肿瘤细胞自发停止表达VEA,同时成为BALB / c宿主中非常弱的移植免疫诱导剂。 VEA的这种损失不是由于这些细胞中脾脏形成灶性病毒或辅助病毒基因组的丢失,因为这两种病毒仍可以从细胞系中回收。

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