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肿瘤坏死因子与γ干扰素在诱导人髓性白血病ML-1细胞分化中的协同作用。

Synergism of tumor necrosis factor and interferon-gamma in induction of differentiation of human myeloblastic leukemic ML-1 cells.

作者信息

Takuma T, Takeda K, Konno K

出版信息

Biochem Biophys Res Commun. 1987 May 29;145(1):514-21. doi: 10.1016/0006-291x(87)91351-9.

DOI:10.1016/0006-291x(87)91351-9
PMID:3109415
Abstract

Natural or recombinant human tumor necrosis factor (TNF) induced NBT-reducing activity of ML-1 cells in a dose-dependent manner. Interferon-gamma (IFN-gamma) induced NBT-reducing activity only marginally. However, when IFN-gamma was combined with TNF, induction of NBT-reducing activity was remarkably increased. IFN-alpha or -beta had almost no effect on the induction of NBT-reducing activity of ML-1 cells, either alone or in combination with TNF. Treatment with both TNF and IFN-gamma synergistically enhanced morphological changes, growth inhibition and activity of Fc receptors, and NBT reduction in ML-1 cells, but not phagocytic activity. The TNF treated cells were classified as macrophage-like by morphology, and by lineage-specific alpha-naphthyl acetate esterase stain. The results indicate that combinations of TNF and IFN-gamma act synergistically in the induction of differentiation of human myeloblastic ML-1 cells.

摘要

天然或重组人肿瘤坏死因子(TNF)以剂量依赖的方式诱导ML-1细胞的NBT还原活性。γ干扰素(IFN-γ)仅轻微诱导NBT还原活性。然而,当IFN-γ与TNF联合使用时,NBT还原活性的诱导显著增加。α或β干扰素单独或与TNF联合使用时,对ML-1细胞NBT还原活性的诱导几乎没有影响。TNF和IFN-γ联合处理可协同增强ML-1细胞的形态变化、生长抑制、Fc受体活性和NBT还原,但不增强吞噬活性。经TNF处理的细胞通过形态学以及谱系特异性α-萘乙酸酯酶染色被归类为巨噬细胞样。结果表明,TNF和IFN-γ组合在诱导人髓母细胞ML-1细胞分化中起协同作用。

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