Chany C, Rousset S, Chany-Fournier F
Tex Rep Biol Med. 1981;41:307-12.
The model of IFN receptor system which we initially proposed in 1973 is now better documented. The receptor system seems to consist of an IFN species specific glycoprotein, which could be the high affinity receptor (30) to which IFN has to bind in order to act. The glycoprotein is thus the activator site. Furthermore, IFN can bind to gangliosides in a non-specific manner. Cooperation between these membrane elements requires the free mobility of the membrane constituents in the plane of the membrane and the integrity of the cytoskeleton. Decay of these constituents during some virus-induced or malignant transformation processes could result in a defect in the synthesis of one of these constituents, causing in parallel a loss of IFN sensitivity. Sodium butyrate, which restores the cytoskeleton, enhances simultaneously the response to IFN. The modulatory effect of IFN on the cell membrane is thus a major step in the regulatory action of IFN on the different phenotypic expressions of the cell. This property of IFN could be one of its principal physiological roles.
我们于1973年最初提出的干扰素受体系统模型，如今已有了更充分的文献记载。该受体系统似乎由一种干扰素特异性糖蛋白组成，它可能是高亲和力受体（30），干扰素必须与之结合才能发挥作用。因此，这种糖蛋白就是激活位点。此外，干扰素能以非特异性方式与神经节苷脂结合。这些膜成分之间的协同作用需要膜成分在膜平面内的自由移动性以及细胞骨架的完整性。在某些病毒诱导或恶性转化过程中，这些成分的衰退可能导致其中一种成分合成缺陷，同时导致对干扰素敏感性的丧失。能恢复细胞骨架的丁酸钠同时增强了对干扰素的反应。因此，干扰素对细胞膜的调节作用是干扰素对细胞不同表型表达进行调节作用的一个主要步骤。干扰素的这一特性可能是其主要生理作用之一。
