Studies on the Potentiating Effect of Deae‐dextran on Interferon Production Induced by Double Stranded Synthetic Polynucleotides **

Dianzani, F.; Gagnoni, S.; Cantagalli, P

doi:10.1111/j.1749-6632.1970.tb53465.x

Cited by 17 publications

(5 citation statements)

References 4 publications

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“…A very similar finding was reported on dextran sulfate, which, under suitable conditions, may abolish the potentiating action of DEAEdextran [7]. However, it is evident that the antagonism can occur independently of the anti-protamine effect, since it is observed in the absence of protamine or with a small amount of non-inducer RNA relative to the amount of protamine.…”

Section: Rna Acting As An Inducer In One Kindsupporting

confidence: 80%

Antagonism of Non‐Inducer Ribonucleic Acid against Induction of Antiviral Cell Resistance and Interferon by Inducer Ribonucleic Acid

Kawade

Matsuyama

Yamamoto

et al. 1972

Japanese Journal of Microbiology

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Various single-stranded RNAs, which do not induce antiviral cell resistance in L and chick embryo cells, were found to antagonize the action of inducer RNAs such as poly(C)¥poly(I). The non-inducing RNA inhibited production of interferon stimulated by inducer RNA, but did not inhibit the action of exogenously added interferon. Two aspects were discerned in the antagonism of non-inducing RNA, namely intrinsic antagonism and anti-protamine effect. The intrinsic antagonism is the one observed in the absence of protamine. The anti-protamine effect is elimination of the potentiating action of protamine on inducing RNA [10] by non-inducing RNA in a large excess over protamine. The relative importance of the two effects will vary depending on the concentrations of protamine and non-inducing RNA used. Non-inducer RNA added to cells pretreated with inducer RNA for 1-3 hr effectively inhibited the development of antiviral cell resistance, but was not very effective when added prior to inducer RNA. RNA from MS2 phage virions was found to be an inducer in chick embryo cell but a non-inducer and antagonist in human embryo lung fibroblasts, indicating that a given RNA may possess both the inducer and the antagonist characters. The induction of interferon by viruses was not significantly inhibited by non-inducing RNA. The results obtained are consistent with an assumption that non-inducing RNA competitively inhibits the binding of inducer RNA to cellular receptor sites, although alternative interpretations are not excluded.

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Section: Rna Acting As An Inducer In One Kindsupporting

confidence: 80%

Antagonism of Non‐Inducer Ribonucleic Acid against Induction of Antiviral Cell Resistance and Interferon by Inducer Ribonucleic Acid

Kawade

Matsuyama

Yamamoto

et al. 1972

Japanese Journal of Microbiology

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“…The rI"-rC" + DEAE-dextran induction of IF in mouse L cells was the precedent for the similar attempts in hamster cells. The addition of almost any amount of DEAE-dextran to rIn-rC" enhanced IF induction in mouse L cells (Dianzani et al, 1970). Whereas the DEAE-dextran/rI"-rC" ratio was not critical in inducing mouse IF, it may be critical in inducing hamster IF.…”

Section: Resultsmentioning

confidence: 90%

Species-specific posttranscriptional regulation of interferon synthesis

Greene¹,

Dieffenbach²,

Yang³

et al. 1980

Biochemistry

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Human fibroblast and Syrian hamster embryo cells were induced to synthesize interferon (IF) with rIn . rCn and rIn . rCn + DEAE-dextran, respectively. Following induction, these cells synthesized IF for only a short time before entering into a repressed state and shutting off the synthesis of IF. Homologous and heterologous whole cell translational systems were developed to investigate the molecular basis for the shut-off of IF synthesis. These systems allowedd for the introduction of exogenous hamster and human IF-mRNAs into intact normal and repressed hamster and human cells via an improved CaCl2 precipitation technique. Human IF-mRNA was translated in normal human and hamster cells and in repressed hamster cells but not in repressed human cells. In contrast, the hamster IF-mRNA was translated in normal human, normal hamster, and repressed human cells but not in repressed hamster cells. These results indicate that a species-specific mechanism inhibiting translation of IF-mRNA is directly responsible for the shut-off of IF synthesis in human fibroblasts and Syrian hamster embryo cells.

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“…If interferon priming is a cell surface (and cell membrane) phenomenon, it should most likely act by increasing the uptake of the interferon inducer (21). In that sense, priming with interferon would be very similar to the potentiation of the interferon response observed after addition of diethylaminoethyl-dextran (10,13).…”

Section: Resultsmentioning

confidence: 97%

Studies on the Mechanism of the Priming Effect of Interferon on Interferon Production by Cell Cultures Exposed to Poly(rI) · Poly(rC)

1973

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Interferon induction by poly(rI) poly(rC) in primary rabbit kidney and mouse L-929 cell cultures was markedly increased if the cells were previously treated with homologous interferon. This priming effect has been established with different times of exposure of the cells to poly(rI) -poly(rC), and was most pronounced for short pulses of contact of the polynucleotide with the cells (10 s, 1 min). Treatment of the cells with pancreatic ribonuclease immediately after their exposure to poly(rI) poly(rC) brought about a relatively greater reduction of the interferon response in interferon-primed cells than it did in unprimed cell cultures. Priming of the cells with interferon did not increase cell-binding of poly(rI) poly(rC), whether this cell-binding was measured quantitatively (by radioactivity, upon exposure of the cells to radiolabeled polymer) or qualitatively (by antiviral activity, by assaying the cell extract for virus plaque reduction). Similarly, interferon priming did not alter the sensitivity of cell-associated poly(rI) poly(rC) to extraneous ribonuclease treatment. Finally, priming with interferon did not decrease the rate of degradation of cell-bound poly(rI). poly(rC) by cellular nucleases nor did it increase the anti-nuclease potency of the cells. The exact mechanism by which previous exposure of the cells to interferon enhances subsequent interferon production, induced by either synthetic polynucleotides or viruses, has not yet been resolved.

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Studies on the Potentiating Effect of Deae‐dextran on Interferon Production Induced by Double Stranded Synthetic Polynucleotides **

Cited by 17 publications

References 4 publications

Antagonism of Non‐Inducer Ribonucleic Acid against Induction of Antiviral Cell Resistance and Interferon by Inducer Ribonucleic Acid

Antagonism of Non‐Inducer Ribonucleic Acid against Induction of Antiviral Cell Resistance and Interferon by Inducer Ribonucleic Acid

Species-specific posttranscriptional regulation of interferon synthesis

Studies on the Mechanism of the Priming Effect of Interferon on Interferon Production by Cell Cultures Exposed to Poly(rI) · Poly(rC)

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