Hanna M G, Tennant R W, Coggin J H
Proc Natl Acad Sci U S A. 1971 Aug;68(8):1748-52. doi: 10.1073/pnas.68.8.1748.
The recovery of spleen cells infected with Rauscher leukemia virus (RLV) and grown in Millipore diffusion chambers, the development of RLV-induced splenomegaly, and the cumulative mortality from a transplanted ascites plasma-cell tumor were all suppressed in young adult BALB/c male mice previously primed at 3-weekly intervals with x-irradiated, syngeneic embryo cells. RLV-induced splenomegaly was also suppressed by adoptive transfer of postpartal spleen cells, as well as spleen cells for animals primed with syngeneic embryo cells. Similar suppressions were not observed in mice primed with neonatal or normal syngeneic cells. Further, injection of fetal cells was not effective in suppressing the immune function of normal spleen cells, as measured by ability to elaborate a primary immunoglobulin M response to heterologous erythrocyte antigen. The results of this study add to the broad spectrum of tumors of experimental animals and man known to contain neoantigens common to fetal cells.
感染劳斯氏白血病病毒（RLV）并在微孔扩散小室中培养的脾细胞的恢复、RLV诱导的脾肿大的发展以及移植性腹水浆细胞瘤的累积死亡率，在先前每隔3周用X射线照射的同基因胚胎细胞进行免疫的年轻成年BALB/c雄性小鼠中均受到抑制。产后脾细胞以及用同基因胚胎细胞免疫的动物的脾细胞的过继转移也抑制了RLV诱导的脾肿大。在用新生或正常同基因细胞免疫的小鼠中未观察到类似的抑制作用。此外，通过对异源红细胞抗原产生原发性免疫球蛋白M反应的能力来衡量，注射胎儿细胞在抑制正常脾细胞的免疫功能方面无效。这项研究的结果增加了已知含有与胎儿细胞共有的新抗原的实验动物和人类肿瘤的范围。
