Jimenez J J, Yunis A A
Department of Medicine, University of Miami School of Medicine, FL 33101.
Blood. 1988 Sep;72(3):1077-80.
We have previously demonstrated that cultured rat chloroleukemia cells, MIA C51, will terminally differentiate to macrophages when treated with rat lung-conditioned medium in vitro and in vivo. In the present study we fractionated rat monocyte-conditioned medium by ultrafiltration according to molecular size. The fraction with molecular weight (mol wt) 30 to 50 Kd containing partially purified granulocyte-macrophage colony-stimulating factor (GM-CSF) activity caused the differentiation of C51 cells to macrophages in vitro and in diffusion chambers in vivo. Treatment of young rats with this fraction aborted the development of chloroleukemia from transplanted C51 cells. In contrast, the fraction with mol wt 10 to 30 Kd containing virtually all the G-CSF activity exhibited no differentiation activity either in vitro or in vivo. It is concluded that in this rat myelogenous leukemia model partially purified GM-CSF but not G-CSF contains the effector molecule(s) causing terminal differentiation of C51 cells and tumor cell rejection.
我们之前已经证明，培养的大鼠氯白血病细胞MIA C51在体外和体内用大鼠肺条件培养基处理时会终末分化为巨噬细胞。在本研究中，我们根据分子大小通过超滤对大鼠单核细胞条件培养基进行分级分离。分子量（mol wt）为30至50 Kd的级分含有部分纯化的粒细胞-巨噬细胞集落刺激因子（GM-CSF）活性，可在体外和体内扩散小室中使C51细胞分化为巨噬细胞。用该级分处理幼鼠可阻止移植的C51细胞引发氯白血病。相比之下，分子量为10至30 Kd的级分几乎包含所有G-CSF活性，在体外或体内均未表现出分化活性。得出的结论是，在该大鼠髓性白血病模型中，部分纯化的GM-CSF而非G-CSF含有导致C51细胞终末分化和肿瘤细胞排斥的效应分子。
