Nooter K, Bentvelzen P
J Natl Cancer Inst. 1976 Jul;57(1):115-8. doi: 10.1093/jnci/57.1.115.
Inoculation of complete Freund's adjuvant (CFA) into BALB/c mice either before or after infection with Rauscher murine leukemia virus (MuLV-R) led to an acceleration of the disease as determined by spleen weight. Treatment with CFA also induced a higher number of spleen erythroblast foci and, in the bone marrow, erythropoietin-independent cells that produced erythroid colonies in vitro. CFA induced in the bone marrow not only an increase in myeloid progenitor cells that can produce colonies in agar, but an ever larger increase in the number of erythroid colony-forming cells. Virus-induced erythroblastosis was probably enhanced by CFA due to the production of many target cells. The more primitive burst-forming cell, which produced large colonies of erythroid cells after 10 days in culture, was also physiologically transformed in MuLV-R-infected mice; bursts could be formed by cells of such animals in the absence of erythropoietin.
在感染劳斯氏小鼠白血病病毒（MuLV-R）之前或之后，将完全弗氏佐剂（CFA）接种到BALB/c小鼠体内，通过脾脏重量测定发现疾病加速发展。用CFA治疗还诱导产生了更多的脾脏成红细胞灶，并且在骨髓中产生了在体外形成红系集落的不依赖促红细胞生成素的细胞。CFA在骨髓中不仅诱导能在琼脂中形成集落的髓系祖细胞数量增加，而且红系集落形成细胞的数量增加得更多。由于产生了许多靶细胞，CFA可能增强了病毒诱导的成红细胞增多症。在MuLV-R感染的小鼠中，在培养10天后产生大量红系细胞集落的更原始的爆式形成细胞也发生了生理转化；此类动物的细胞在没有促红细胞生成素的情况下也能形成爆式集落。
