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首页> 外文期刊>Infection and immunity >Endotoxin-induced serum factor that stimulates gamma interferon production.
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Endotoxin-induced serum factor that stimulates gamma interferon production.

机译：内毒素诱导的血清因子，可刺激γ干扰素的产生。

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Serum from Mycobacterium bovis BCG-infected mice that had been challenged with lipopolysaccharide (LPS) exhibited a marked ability to induce gamma interferon (IFN-gamma) in cultures of spleen cells of normal mice in the presence of interleukin-2 (IL-2). The inducing activity became detectable in the circulatory system about 90 min after LPS challenge, disappeared at around 5 h, and was observable upon 640x dilution of the serum. Addition of monoclonal anti-IL-2 receptor antibody to the culture inhibited the induction by the serum. The activity induced high levels of IFN-gamma even in nylon wool-nonadherent cells, while concanavalin A failed to do so. Serum from uninfected mice challenged with LPS contained no such activity. The molecular weight of the active substance, estimated by gel filtration, was about 70,000. There were pronounced differences among mouse strains in the activities of the sera prepared, which paralleled the amounts of IFN-gamma produced in vivo. However, the levels of IFN-gamma produced in whole spleen cells and in nylon wool-nonadherent cells from mice of various strains were the same when stimulated with competent serum. These results indicate the existence of an unidentified factor that induces IFN-gamma in cooperation with IL-2 in macrophage-depleted splenocytes. They also suggest that IFN-gamma production in vivo is not genetically controlled at the lymphocyte level but, rather, at the level of synthesis of the unknown factor.
机译：在存在白介素2（IL-2）的情况下，来自牛分枝杆菌BCG感染小鼠的血清经脂多糖（LPS）攻击后，在正常小鼠脾细胞培养物中表现出明显的诱导γ干扰素（IFN-γ）的能力。 。在LPS激发后约90分钟，在循环系统中可检测到诱导活性，在约5小时时消失，并且在将血清稀释640倍后可观察到。向培养物中添加单克隆抗IL-2受体抗体抑制了血清的诱导。即使在尼龙毛非粘附细胞中，该活性也诱导了高水平的IFN-γ，而伴刀豆球蛋白A却没有。来自未感染小鼠的经LPS攻击的血清不包含此类活性。通过凝胶过滤估计的活性物质的分子量为约70000。小鼠品系之间在制备的血清活性方面存在明显差异，这与体内产生的IFN-γ数量相当。然而，当用感受态血清刺激时，来自不同品系小鼠的整个脾细胞和尼龙羊毛非贴壁细胞中产生的IFN-γ水平是相同的。这些结果表明在巨噬细胞耗竭的脾细胞中存在与IL-2协同诱导IFN-γ的未知因子。他们还表明，体内IFN-γ的产生不是在淋巴细胞水平上遗传控制的，而是在未知因子合成水平上的遗传控制。

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