Silver J, Teich N
J Exp Med. 1981 Jul 1;154(1):126-37. doi: 10.1084/jem.154.1.126.
Bone marrow chimeras were formed containing mixtures of DBA/2 (Fv-2ss, Hbbdd) and B10.D2 (Fv-2rr, Hbbss) bone marrow. When these mice were infected with the polycythemia-inducing strain of Friend virus, erythropoiesis was stimulated, but the proportion of B10.D2 hemoglobin fell rapidly and newly synthesized hemoglobin was essentially all of the DBA/2 type. The treatment of infected polycythemic chimeras with phenylhydrazine lowered the hematocrit and restored the synthesis of B10.D2 hemoglobin. These results imply that B10.D2 erythroid precursors are intrinsically resistant to Friend virus-stimulated erythropoiesis. The experiments also suggest that virus-stimulated erythropoiesis is not mediated by a factor or cell-cell interactions, unless such factors or interactions do not act across strain barriers.
构建了含有DBA/2(Fv - 2ss,Hbbdd)和B10.D2(Fv - 2rr,Hbbss)骨髓混合物的骨髓嵌合体。当这些小鼠感染多嗜性贫血诱导型Friend病毒时,红细胞生成受到刺激,但B10.D2血红蛋白的比例迅速下降,新合成的血红蛋白基本上全是DBA/2型。用苯肼处理感染多嗜性贫血的嵌合体可降低血细胞比容并恢复B10.D2血红蛋白的合成。这些结果表明,B10.D2红系前体细胞对Friend病毒刺激的红细胞生成具有内在抗性。这些实验还表明,病毒刺激的红细胞生成不是由一种因子或细胞间相互作用介导的,除非这种因子或相互作用不能跨越品系障碍发挥作用。