Mechanisms of DEAE-Dextran Enhancement of Polynucleotide Induction of Interferon

Abstract
The present results demonstrate that, in the presence of an excess of DEAE-dx, In does not precipitate but it complexes with the polycation in a way which makes it resistant to pancreatic RNase. The formation of this type of complex may occur with other polycationic substances. Preliminary experiments show that high concentrations of neomycin produce a soluble complex, and poly-d-lysine at a change ratio of >30:1 also produces a soluble InCn-polycation (J. M. Rice, personal communication). It was also found that the induction of IF by the RNase-resistant complex was potentiated by the addition of DEAE-dx to the cell cultures. This indicates that protection of InCn against enzymatic degradation is not the sole mechanism by which IF production can be enhanced by DEAE-dx. It implies that DEAE-dx causes a large part of its enhancement by an effect on cells. Conceivably this could involve increased cellular uptake of the InCn as DEAE-dx does for other RNAs (5-7) but the need for such uptake has not been established. Additional evidence for a cell-mediated action of DEAE-dx comes from the previous observation that pretreatment of cells with DEAE-dx gave a maximal enhancing effect which could be abolished by brief contact of the treated cells with the polyanionic dextran sulfate (2).

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