Kuzumaki N, Moriuchi T, Kodama T, Kobayashi H
J Immunol. 1976 Oct;117(4):1250-5.
Newborn rats given injections of low doses of Friend lymphatic leukemia virus subsequently developed hemolytic anemia characterized by production of antierythrocyte autoantibody. Electron microscopy showed C-type virus particles budding from the cell membrane not only of lymphoid cells but also of erythrocyte percursor cells in bone marrow and spleen, suggesting that the erythroid cells were infected by the virus. In addition, erythrocyte precursor cells expressed virus-induced cell surface antigens detected by cytotoxicity tests. Normal syngeneic rats preimmunized with a Friend lymphatic leukemia virusinduced tumor and subsequently inoculated with bone marrow, spleen cells, or reticulocyte-rich fraction derived from other rats injected with high doses of the virus at birth produced cytotoxic antibody to the virus-induced tumor and antierythrocyte autoantibody. In contrast, rats subsequently inoculated with virus-infected thymus or lymph node cells produced cytotoxic antibody but not antierythrocyte autoantibody. These results indicate that "xenogenization," previously shown for tumor cells and normal lymphoid cells, is also observed for rat erythroid cells and, further, that xenogenization of erythroid cells by Friend lymphatic leukemia virus is one of the most important factors in induction of autoimmune hemolytic anemia.
给新生大鼠注射低剂量的弗瑞德淋巴白血病病毒后，它们随后出现了以抗红细胞自身抗体产生为特征的溶血性贫血。电子显微镜显示，C型病毒颗粒不仅从淋巴细胞的细胞膜上出芽，也从骨髓和脾脏中的红细胞前体细胞的细胞膜上出芽，这表明红系细胞受到了病毒感染。此外，红细胞前体细胞表达了通过细胞毒性试验检测到的病毒诱导的细胞表面抗原。用弗瑞德淋巴白血病病毒诱导的肿瘤预先免疫的正常同基因大鼠，随后接种来自出生时注射高剂量该病毒的其他大鼠的骨髓、脾细胞或富含网织红细胞的部分，会产生针对病毒诱导肿瘤的细胞毒性抗体和抗红细胞自身抗体。相比之下，随后接种病毒感染的胸腺或淋巴结细胞的大鼠产生了细胞毒性抗体，但没有产生抗红细胞自身抗体。这些结果表明，先前在肿瘤细胞和正常淋巴细胞中观察到的“异种化”现象，在大鼠红系细胞中也存在，而且，弗瑞德淋巴白血病病毒导致的红系细胞异种化是诱导自身免疫性溶血性贫血的最重要因素之一。
