Hemmi H, Nakamura T, Shimizu Y, Sugamura K
Department of Bacteriology, Tohoku University School of Medicine, Sendai, Japan.
J Natl Cancer Inst. 1989 Jun 21;81(12):952-6. doi: 10.1093/jnci/81.12.952.
Two lymphokines that contribute to induction of cell differentiation in promyelocytic HL-60 leukemia cells by human T-cell lymphoma HUT-102 cells were identified previously. The lymphokines identified in the differentiation-inducing preparation were interferon-gamma (IFN-gamma) and lymphotoxin. To determine the remaining component(s) of this differentiation-inducing activity, we used gene-cloned (recombinant) forms and antibodies of lymphokines. The differentiation-inducing activity of the HUT-102 cells was not completely neutralized by the antibodies, suggesting that an additional lymphokine(s) is involved. Granulocyte-macrophage colony-stimulating factor (GM-CSF) in combination with retinoic acid induced differentiation of the HL-60 cells in a dose-dependent manner. Furthermore, the activity of the differentiation-inducing factors was partially inhibited by anti-GM-CSF antibody and completely inhibited by the combination of antibodies to lymphotoxin, IFN-gamma, and GM-CSF. These results indicate that, in addition to IFN-gamma and lymphotoxin, GM-CSF is the third major component released by HUT-102 cells for inducing differentiation of HL-60 cells.
先前已鉴定出两种由人T细胞淋巴瘤HUT-102细胞产生的、有助于诱导早幼粒细胞HL-60白血病细胞分化的淋巴因子。在诱导分化制剂中鉴定出的淋巴因子是γ干扰素（IFN-γ）和淋巴毒素。为了确定这种诱导分化活性的其余成分，我们使用了基因克隆（重组）形式的淋巴因子和抗体。HUT-102细胞的诱导分化活性并未被抗体完全中和，这表明还涉及一种额外的淋巴因子。粒细胞-巨噬细胞集落刺激因子（GM-CSF）与视黄酸联合以剂量依赖的方式诱导HL-60细胞分化。此外，诱导分化因子的活性被抗GM-CSF抗体部分抑制，并被针对淋巴毒素、IFN-γ和GM-CSF的抗体联合完全抑制。这些结果表明，除了IFN-γ和淋巴毒素外，GM-CSF是HUT-102细胞释放的用于诱导HL-60细胞分化的第三种主要成分。
