Raineri I, Huang T T, Epstein C J, Epstein L B
Cancer Research Institute, University of California, San Francisco, USA.
J Interferon Cytokine Res. 1996 Jan;16(1):61-8. doi: 10.1089/jir.1996.16.61.
Manganese superoxide dismutase (MnSOD) is induced by interferon-gamma (IFN-gamma) in various cell lines. To determine whether MnSOD plays a role in the antiviral action of IFN-gamma, we employed an antisense strategy to inhibit the expression of MnSOD in the human melanoma cell line, A375. Three antisense-containing clones that exhibited reduced induction of MnSOD were investigated with respect to their response to the antiviral protective effects of IFN-gamma and IFN-alpha. We observed a striking decrease in the ability of IFN-gamma to protect antisense clones from vesicular stomatitis virus infection (VSV). The IFN-alpha induced antiviral state was also impaired, but to a lesser degree than was observed with IFN-gamma. We excluded the possibility that these effects were caused by a higher sensitivity of the antisense cells to VSV itself and found that the antisense clones actually were less sensitive to VSV. Therefore, we conclude that MnSOD is involved in the establishment of the IFN-gamma-induced antiviral state and to a lesser degree in the antiviral actions of IFN-gamma.
锰超氧化物歧化酶（MnSOD）在多种细胞系中由γ干扰素（IFN-γ）诱导产生。为确定MnSOD是否在IFN-γ的抗病毒作用中发挥作用，我们采用反义策略抑制人黑色素瘤细胞系A375中MnSOD的表达。针对三个显示出MnSOD诱导减少的含反义序列的克隆，研究了它们对IFN-γ和IFN-α抗病毒保护作用的反应。我们观察到IFN-γ保护反义克隆免受水泡性口炎病毒（VSV）感染的能力显著下降。IFN-α诱导的抗病毒状态也受到损害，但程度低于IFN-γ。我们排除了这些效应是由反义细胞对VSV本身更高的敏感性引起的可能性，并发现反义克隆实际上对VSV的敏感性较低。因此，我们得出结论，MnSOD参与IFN-γ诱导的抗病毒状态的建立，且在较小程度上参与IFN-γ的抗病毒作用。
