Chany C, Grégoire A, Vignal M, Lemaitre-Moncuit J, Brown P, Besançon F, Suarez H, Cassingena R
Proc Natl Acad Sci U S A. 1973 Feb;70(2):557-61. doi: 10.1073/pnas.70.2.557.
Dose-response curves of interferons in different sensitive cells are regularly sigmoidal. In somatic monkey-mouse hybrid cells, however, a significant decrease in the slope of the curve for primate interferon was observed, while the dose-response effect was unaltered for mouse interferon. High concentrations of primate interferon were 10- to 100-times less effective in hybrid clones than in parental monkey CV-1 cells; at low concentrations the antiviral effect was 10- to 20-times higher in hybrid clones than in the parental cells. The receptor(s) for primate interferon located on the cell membrane was destroyed by trypsin but not by EDTA. Similarly, acid pH inactivated these receptor sites. We, thus, postulate that the antiviral effect is, at least partially, related to the amount of interferon taken up by the cells. Uptake could be conditioned by active cooperation of two cell-specific factors: a receptor and an activator. The activator might be missing or inactivated for primate interferon in the hybrid cells. We suggest that the putative antiviral protein is not cell-species specific, and that information for its synthesis in the hybrid cells might be located on a mouse rather than a monkey chromosome.
干扰素在不同敏感细胞中的剂量反应曲线通常呈S形。然而，在体细胞猴-鼠杂交细胞中，观察到灵长类干扰素曲线的斜率显著下降，而小鼠干扰素的剂量反应效应未改变。高浓度的灵长类干扰素在杂交克隆中的效力比在亲代猴CV-1细胞中低10至100倍；在低浓度时，杂交克隆中的抗病毒效应比亲代细胞高10至20倍。位于细胞膜上的灵长类干扰素受体被胰蛋白酶破坏，但不被EDTA破坏。同样，酸性pH使这些受体位点失活。因此，我们推测抗病毒效应至少部分与细胞摄取的干扰素量有关。摄取可能受两种细胞特异性因子的积极协作调节：一种受体和一种激活剂。杂交细胞中灵长类干扰素的激活剂可能缺失或失活。我们认为假定的抗病毒蛋白不是细胞物种特异性的，并且其在杂交细胞中合成的信息可能位于小鼠而非猴染色体上。
