Yoshida I, Azuma M
J Interferon Res. 1985 Winter;5(1):1-10. doi: 10.1089/jir.1985.5.1.
PR-RK cells, which were derived from RK-13 cells by repeated treatment with a copolymer of polyriboinosinic acid and polyribocytidylic acid (poly rI:rC), were resistant to the cytotoxic effect of poly rI:rC, and could not produce interferon when exposed to poly rI:rC alone. These characteristics of PR-RK cells have not reversed for more than 40 passages of the cells in medium without poly rI:rC. Poly rI:rC was adsorbed on PR-RK cells at a rate of 60 to 70% of its adsorption to RK-13 cells. On the other hand, PR-RK cells could produce a low level of interferon when they were induced by a poly rI:rC-DEAE dextran complex, by poly rI:rC and metabolic inhibitors (superinduction), by poly rI:rC and pretreatment with interferon (priming), and by Newcastle disease virus. Interferon production in RK-13 cells in response to poly rI:rC or poly rI:rC-DEAE dextran complex was inhibited by pretreatment of the cells with anti-RK-13 cell serum and anti-RK-13 cell serum absorbed with PR-RK cells. These results suggest that PR-RK cells are deficient in the receptor for poly rI:rC, and that poly rI:rC can adsorb onto the cell membrane nonspecifically, acting as a weak inducer when transcriptional control in cells is affected by superinduction or priming. Only about 30% of the poly rI:rC adsorbed on RK-13 cells may be specific binding, participating in normal interferon induction.
PR-RK细胞由RK-13细胞经聚肌苷酸-聚胞苷酸共聚物（poly rI:rC）反复处理后获得，对poly rI:rC的细胞毒性作用具有抗性，单独暴露于poly rI:rC时不能产生干扰素。在不含poly rI:rC的培养基中传代40多次后，PR-RK细胞的这些特性并未逆转。与RK-13细胞相比，poly rI:rC以其吸附量60%至70%的速率吸附在PR-RK细胞上。另一方面，当PR-RK细胞由poly rI:rC-DEAE葡聚糖复合物、poly rI:rC与代谢抑制剂（超诱导）、poly rI:rC与干扰素预处理（启动）以及新城疫病毒诱导时，它们能产生低水平的干扰素。用抗RK-13细胞血清和经PR-RK细胞吸收的抗RK-13细胞血清预处理RK-13细胞，可抑制其对poly rI:rC或poly rI:rC-DEAE葡聚糖复合物产生干扰素。这些结果表明，PR-RK细胞缺乏poly rI:rC受体，并且poly rI:rC可以非特异性地吸附到细胞膜上，当细胞中的转录控制受到超诱导或启动影响时，作为一种弱诱导剂起作用。吸附在RK-13细胞上的poly rI:rC中只有约30%可能是特异性结合，参与正常的干扰素诱导。
