Abstract
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 preptreatment 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.
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