Dorsch M, Hock H, Kunzendorf U, Diamantstein T, Blankenstein T
Institut für Immunologie, Universitätsklinikum Steglitz, Freie Universität Berlin, FRG.
Eur J Immunol. 1993 Jan;23(1):186-90. doi: 10.1002/eji.1830230129.
In order to analyze the effect of a high local concentration of macrophage colony-stimulating factor (M-CSF; CSF-1) on tumor growth, the plasmacytoma cell line J558L was transfected with the human M-CSF gene and injected into syngeneic BALB/c mice. In contrast to the parental tumors, M-CSF transfectants were heavily infiltrated by macrophages as evidenced by immunohistochemistry with antibodies to Mac-1 and Mac-3 and by isolation of the macrophages from the tumor. Nevertheless, tumor growth was only slightly affected by M-CSF and M-CSF-producing cells grew as tumor in all cases. The growth retardation of M-CSF-producing cells varied depending on the experiment and seemed to be due to an indirect effect because the growth rate of the cells in vitro had not changed upon gene transfer. Attempts to activate the tumor-infiltrating macrophages for tumor suppression by systemic application of interferon-gamma and/or lipopolysaccharide were not successful. Altogether, our results suggest that M-CSF is a potent chemoattractant for macrophages in vivo but alone is not sufficient to activate these macrophages for tumoricidal activity.
为了分析高局部浓度的巨噬细胞集落刺激因子（M-CSF；CSF-1）对肿瘤生长的影响，将浆细胞瘤细胞系J558L用人类M-CSF基因转染，并注射到同基因的BALB/c小鼠体内。与亲代肿瘤不同，通过用抗Mac-1和Mac-3抗体进行免疫组织化学以及从肿瘤中分离巨噬细胞证明，M-CSF转染瘤被巨噬细胞大量浸润。然而，肿瘤生长仅受到M-CSF的轻微影响，并且产生M-CSF的细胞在所有情况下都像肿瘤一样生长。产生M-CSF的细胞的生长迟缓因实验而异，似乎是由于间接作用，因为基因转移后细胞在体外的生长速率并未改变。通过全身应用干扰素-γ和/或脂多糖来激活肿瘤浸润巨噬细胞以抑制肿瘤的尝试未成功。总之，我们的结果表明，M-CSF在体内是巨噬细胞的有效趋化因子，但单独不足以激活这些巨噬细胞产生杀肿瘤活性。
