Blalock J E, Georgiades J, Johnson H M
J Immunol. 1979 Mar;122(3):1018-21.
Mouse immune-type interferon (type II), a lymphokine, caused the transfer of viral resistance from mouse L cells to human WISH cells. The interferon was incapable of protecting WISH cells in the absence of L cells. The transfer of viral resistance occurred with interferon preparations of various specific activities, and was in proportion to the interferon concentration in the preparations. The transferred resistance had the characteristics of an interferon-induced antiviral state in that it was blocked by actinomycin D, effective against different types of viruses, and resulted from an action on the cell rather than on the virus. Mouse immune-type interferon was more efficient than virus-type (type I) at eliciting the transfer of protection. The transfer phenomenon may represent a mechanism for amplification of the interferon system as a host defense against viral infection. Further, it serves as a model for studying the mechanism of lymphokine-induced transfer of information between cells.
小鼠免疫型干扰素(Ⅱ型),一种淋巴因子,可使病毒抗性从小鼠L细胞转移至人WISH细胞。在没有L细胞的情况下,该干扰素无法保护WISH细胞。病毒抗性的转移发生在具有各种比活性的干扰素制剂中,且与制剂中的干扰素浓度成正比。转移的抗性具有干扰素诱导的抗病毒状态的特征,即它被放线菌素D阻断,对不同类型的病毒有效,并且是由对细胞而非病毒的作用导致的。在引发保护转移方面,小鼠免疫型干扰素比病毒型(Ⅰ型)更有效。这种转移现象可能代表了干扰素系统作为宿主抗病毒感染防御机制的一种放大机制。此外,它还作为研究淋巴因子诱导细胞间信息转移机制的模型。