Broxmeyer H E, Ralph P, Gilbertson S, Margolis V B
Cancer Res. 1980 Nov;40(11):3928-33.
Neonatal and adult BALB/c mice were investigated in a longitudinal study for the acquisition of leukemia-associated inhibitory activity (LIA) interactions after inoculation with Abelson virus in vivo. Within 2 to 4 days after virus infection, the granulocyte-macrophage colony-forming cells from the bone marrow and spleen of the infected mice became insensitive to inhibition by LIA, even though colony morphology appeared normal. Shortly after, or simultaneously with, the detection of the colony-forming cell resistance phenomenon, LIA was found in bone marrow, spleen, and thymus cells. The abnormal interactions appeared to be related to induction of lymphoma in BALB/c neonates and to a lymphoproliferative disease in adult BALB/c mice. In contrast, normal cellular interactions were noted in adult C57BL/6 mice which were not susceptible to the Abelson disease after virus inoculation and in untreated neonatal and adult BALB/c and adult C57BL/6 mice. Their colony-forming cells were sensitive to inhibition by LIA, and no LIA was detected in their bone marrow, spleen, and thymus cells. The abnormal cellular interactions are similar to those noted in human leukemia, lymphoma, and "preleukemia." This suggests that Abelson virus-infected mice can serve as a model for the study of LIA interactions.
在一项纵向研究中,对新生和成年BALB/c小鼠进行了调查,以研究其在体内接种阿贝尔森病毒后白血病相关抑制活性(LIA)相互作用的获得情况。在病毒感染后的2至4天内,受感染小鼠骨髓和脾脏中的粒细胞-巨噬细胞集落形成细胞对LIA的抑制作用变得不敏感,尽管集落形态看起来正常。在检测到集落形成细胞抗性现象后不久或同时,在骨髓、脾脏和胸腺细胞中发现了LIA。这种异常相互作用似乎与BALB/c新生小鼠淋巴瘤的诱导以及成年BALB/c小鼠的淋巴细胞增生性疾病有关。相比之下,在接种病毒后不易患阿贝尔森病的成年C57BL/6小鼠以及未处理的新生和成年BALB/c及成年C57BL/6小鼠中,观察到正常的细胞相互作用。它们的集落形成细胞对LIA的抑制敏感,并且在其骨髓、脾脏和胸腺细胞中未检测到LIA。这种异常的细胞相互作用类似于在人类白血病、淋巴瘤和“白血病前期”中观察到的情况。这表明阿贝尔森病毒感染的小鼠可作为研究LIA相互作用的模型。