De Clercq E, De Somer P
J Gen Virol. 1975 Apr;27(1):35-44. doi: 10.1099/0022-1317-27-1-35.
Interferon-treated L cells exhibit a specific enhanced susceptibility to the cytotoxic and interferon inducing activities of double-stranded RNAs such as poly(1). poly(C). These activities remained closely linked through widely varying assay conditions, involving, for example, different time anddosage schedules of poly(1). poly (C),suggesting that there is at least one common step in the mechanisms leading to interferon formation and toxicity in interferon-primed cells exposed to poly(1).poly(C). However, some procedures such as addition of metabolic inhibitors (actinomycin D, cycloheximide) and repeated administration of poly(1).poly(C) suppressed the interferon inducing capacity of poly(1).poly(C) without a concomitant decrease of toxicity. Other procedures such as brief treatment of the cells with interferon or DEAE-dextran permitted full expression of the interferon inducing activity of poly(1).poly(C) without any sign of toxicity. The latter results suggest that the mechanisms underlying interferon production and toxicity of poly(1).poly(C) in interferon-treated L cells diverge from a certain point onward.
经干扰素处理的L细胞对双链RNA（如聚肌苷酸-聚胞苷酸）的细胞毒性和干扰素诱导活性表现出特定的增强敏感性。通过广泛变化的测定条件，这些活性仍紧密相关，例如涉及聚肌苷酸-聚胞苷酸不同的时间和剂量方案，这表明在暴露于聚肌苷酸-聚胞苷酸的经干扰素预处理的细胞中，导致干扰素形成和毒性的机制中至少有一个共同步骤。然而，一些操作，如添加代谢抑制剂（放线菌素D、环己酰亚胺）和重复给予聚肌苷酸-聚胞苷酸，会抑制聚肌苷酸-聚胞苷酸的干扰素诱导能力，而毒性并未随之降低。其他操作，如用干扰素或DEAE-葡聚糖短暂处理细胞，可使聚肌苷酸-聚胞苷酸的干扰素诱导活性充分表达，且无任何毒性迹象。后一结果表明，在经干扰素处理的L细胞中，聚肌苷酸-聚胞苷酸产生干扰素和毒性的机制从某一点开始出现分歧。
