Cheung D L, Hart P H, Vitti G F, Whitty G A, Hamilton J A
University of Melbourne, Department of Medicine, Royal Melbourne Hospital, Parkville, Australia.
Immunology. 1990 Sep;71(1):70-5.
Stimulated human monocytes/macrophages are a source of interleukin-6 (IL-6), which is a likely mediator involved in immune and inflammatory reactions. The means to control production of IL-6 by these cells could therefore have therapeutic applications. We report here, for lipopolysaccharide (LPS)-stimulated human monocytes in vitro, that the lymphokine, interferon-gamma (IFN-gamma) (100 U/ml), enhanced the level of IL-6 activity, whereas another lymphokine, interleukin-4 (IL-4) (greater than or equal to 0.1 U/ml; greater than or equal to 1.2 x 10(-11) M), suppressed it. The effects of the two lymphokines were manifested at the level of mRNA. The action of the IL-4 was similar to that of the glucocorticoid, dexamethasone, but observed at a lower molar concentration. Such regulation of monocyte IL-6 activity is similar to that found previously for interleukin-1 (IL-1) and tumour necrosis factor-alpha (TNF-alpha) synthesis.
受刺激的人单核细胞/巨噬细胞是白细胞介素-6（IL-6）的来源，IL-6可能是参与免疫和炎症反应的介质。因此，控制这些细胞产生IL-6的方法可能具有治疗应用价值。我们在此报告，对于体外脂多糖（LPS）刺激的人单核细胞，淋巴因子γ干扰素（IFN-γ）（100 U/ml）可提高IL-6活性水平，而另一种淋巴因子白细胞介素-4（IL-4）（≥0.1 U/ml；≥1.2×10⁻¹¹ M）则抑制该活性。这两种淋巴因子的作用在mRNA水平表现出来。IL-4的作用与糖皮质激素地塞米松相似，但在较低摩尔浓度下即可观察到。单核细胞IL-6活性的这种调节与先前发现的白细胞介素-1（IL-1）和肿瘤坏死因子-α（TNF-α）合成的调节相似。
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