Pitha P M, Vengris V E, Reynolds F H
J Supramol Struct. 1976;4(4):467-73. doi: 10.1002/jss.400040405.
The mechanism of interferon action in human fibroblasts has been studied by use of both antisera to human fibroblast interferon and the antisera to the surface of human fibroblast cell. The anti-interferon serum completely neutralized the antiviral effect of human fibroblast interferon. Interferon antiserum prevented the intracellular antiviral state from developing when added to the medium of the cells in which interferon synthesis had already been induced by poly (I-C). This suggests that development of the antiviral state involves interferon interaction with the external part of the producing cell. Treatment with the serum directed against the surface of human fibroblast cells failed to inhibit the antiviral activity of human interferon in these cells. In addition, the effect of gangliosides on the antiviral activity of human interferon was studied and it was found that human interferon binds to gangliosides and that this interaction leads to inactivation of the antiviral effect of interferon. Pretreatment of human fibroblasts with gangliosides had no effect on the sensitivity of these cells to exogenous interferon.
通过使用抗人成纤维细胞干扰素血清和抗人成纤维细胞表面血清,对人成纤维细胞中干扰素的作用机制进行了研究。抗干扰素血清完全中和了人成纤维细胞干扰素的抗病毒作用。当将干扰素抗血清添加到已经由聚(I-C)诱导干扰素合成的细胞培养基中时,它阻止了细胞内抗病毒状态的发展。这表明抗病毒状态的发展涉及干扰素与产生细胞外部部分的相互作用。用针对人成纤维细胞表面的血清处理未能抑制这些细胞中人类干扰素的抗病毒活性。此外,研究了神经节苷脂对人干扰素抗病毒活性的影响,发现人干扰素与神经节苷脂结合,并且这种相互作用导致干扰素抗病毒作用的失活。用神经节苷脂预处理人成纤维细胞对这些细胞对外源干扰素的敏感性没有影响。