Barton B E, Jackson J V, Lee F, Wagner J
Department of Immunology, Schering-Plough Research Institute, Kenilworth, NJ 07033.
Cytokine. 1994 Mar;6(2):147-53. doi: 10.1016/1043-4666(94)90036-1.
Oncostatin M was found to stimulate the IL-6-addicted hybridoma line B9. Leukaemia inhibitory factor did not stimulate proliferation of this line. Both of these factors bind to the gp130 of the IL-6 receptor. In another cell line that is stimulated by LIF (DA.1), neither IL-6 nor oncostatin M stimulated proliferation. Previously it had been thought that the gp130 alone is sufficient to bind ligand and transduce signal and that oncostatin M could bind to and activate the LIF receptor, but these data show this is not always the case. Mice primed with Pristane were found to have IL-6 in their sera and peritoneal fluid only at a few time points following Pristane treatment; this was determined by IL-6-specific ELISA. When the same samples were analysed on IL-6-addicted B9 cells, stimulatory activity was found at all time points. When the Pristane-primed samples were assayed for oncostatin M activity in the A375 melanoma assay, there was oncostatin M activity at various time points. IL-6 did not have activity on the A375 cells. These data indicate that oncostatin M play a role in the generation of plasmacytoma in vivo.
研究发现抑瘤素M可刺激对白细胞介素-6(IL-6)成瘾的杂交瘤细胞系B9。白血病抑制因子不能刺激该细胞系的增殖。这两种因子均与IL-6受体的gp130结合。在另一种受白血病抑制因子(LIF)刺激的细胞系(DA.1)中,IL-6和抑瘤素M均不能刺激其增殖。此前人们认为仅gp130就足以结合配体并转导信号,并且抑瘤素M可以结合并激活LIF受体,但这些数据表明情况并非总是如此。发现用 pristane 预处理的小鼠仅在 pristane 处理后的几个时间点血清和腹腔液中有IL-6;这是通过IL-6特异性酶联免疫吸附测定法确定的。当在对IL-6成瘾的B9细胞上分析相同样本时,在所有时间点均发现有刺激活性。当在A375黑色素瘤试验中检测用pristane预处理的样本的抑瘤素M活性时,在不同时间点均有抑瘤素M活性。IL-6对A375细胞没有活性。这些数据表明抑瘤素M在体内浆细胞瘤的发生中起作用。