Specific binding of poly(I) · poly(C) to the membrane of murine B lymphocyte subsets

Diamantstein, T; Blitstein-Willinger, E

doi:10.1002/eji.1830081213

Cited by 9 publications

(3 citation statements)

References 9 publications

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“…There were no signs of extensive parenchymal damage or organ dysfunction associated with the cellular infiltration with the exception of the liver in animals treated with 100 mg/kg of CGP 69846A. Immune stimulatory effects have been reported previously (Henry et ai, 1997c;Monteith et ai, 1997;Sarmiento et ai, 1994) and are probably related to the polyanionic composition of these compounds (Diamantstein and Blistein-Willinger, 1978;Diamantstein et ai, 1971;Homan et ai, 1972). Polyanionic molecules, including P=S ODNs, are known to stimulate B-cell proliferation and some of the immune responses observed in rodents may be the result of this effect (Pisetsky and Reich, 1994).…”

Section: Discussionmentioning

confidence: 50%

Preclinical Evaluation of the Effects of a Novel Antisense Compound Targeting C-rafKinase in Mice and Monkeys

Monteith

Geary

Leeds

et al. 1998

Toxicological Sciences

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Section: Discussionmentioning

confidence: 50%

Preclinical Evaluation of the Effects of a Novel Antisense Compound Targeting C-rafKinase in Mice and Monkeys

Monteith

Geary

Leeds

et al. 1998

Toxicological Sciences

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“…Further work with these cells indicates that a 60-kDa protein can be detected that is a specific receptor for poly(I)-poly(C) (42). Specific binding of poly(I)-poly(C) has also been reported on murine B cells (43). However, Scatchard analysis of specific binding was not done in either of these studies.…”

Section: Discussionmentioning

confidence: 87%

Cyclic AMP mediates the direct antiproliferative action of mismatched double-stranded RNA.

Hubbell

Boyer

Roane

et al. 1991

Proc. Natl. Acad. Sci. U.S.A.

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Previous experiments have demonstrated that double-stranded RNAs (dsRNAs) can exert an antiproliferative effect on human tumor cells, independent of interferon (lEN) induction. However, the mechanism by which dsRNAs inhibit tumor growth has not been elucidated. As a first step in determining the molecular events responsible for growth arrest, we have explored the role of signal transduction through the cAMP system in the antiproliferative effect of the mismatched dsRNA, r(I),Wr(CI2,U). (Ampligen). These studies utilized the human glioma cell line A1235, which does not produce detectable levels of IFN-a, -P, or -y in response to mismatched dsRNA treatment. Treatment of A1235 cells with mismatched dsRNA in combination with either 1-(5-isoquinolinesulfonyl)-2-methylpiperazine (H-7), which inhibits cAMP-dependent protein kinase and protein kinase C, or N-(2-guanidinoethyl)-5-isoquinolinesulfonamide (HA1004), which preferentially inhibits the cAMP-dependent protein kinase, yielded an antagonism of the mismatched dsRNAinduced antiproliferative effect. Measurement of adenylate cyclase activation showed a dose-dependent increase in activity at antiproliferative mismatched dsRNA concentrations, but not at lower, nonantiproliferative doses. This increase in activity was rapid, seen as early as 30 sec after initiation of treatment, and it was sustained at peak levels for 1-2 hr. Analysis of the intracellular cAMP concentration gave similar kinetics of induction. Exposure of cells to the stable cAMP analogue dibutyryl cAMP yielded dose-dependent inhibition of cell growth. The cAMP phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine also inhibited proliferation. In contrast, neither H-7 nor HA1004 had an effect on growth inhibition induced by human natural IFN-a treatment. In addition, antiproliferative doses of IFN-a did not increase cAMP concentrations. These results indicate that the cAMP system is utilized by mismatched dsRNA as an early signal transduction mechanism for growth control. Furthermore, the antiproliferative effects induced by mismatched dsRNA and IFN can occur by different mechanisms of action.Interferons (IFNs) have pleiotropic effects on cells in both tissue culture and in vivo, including antiviral, antiproliferative, and immunomodulatory effects (1-3). Although the biochemical mechanisms of the actions of IFN are not known, it is known that the effects are receptor mediated (4-6). Since the IFN is degraded shortly after its interaction with the receptor and internalization (4-6), receptorassociated signal transduction mechanisms may play a role in IFN-induced events. Conflicting results have been reported for the role of the cAMP signal transduction system in IFN-induced growth inhibition. Although it has been suggested that IFN-associated increases in intracellular cAMP concentration may mediate the inhibition of DNA synthesis (7,8), other reports have indicated that cAMP is not related to DNA synthesis or growth inhibition (9-13).Double-stranded (ds) RNAs are potent inducers of IFNs (14) an...

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“…Dextran sulfate (Swain et al, 1983) and poly(IC) (polyinosinic polycytidylic acid; Diamantstein and Blitstein-Willinger, 1978) are weak polyclonal activators and therefore are infrequently utilized. However, they may be useful for testing the effects of various co-stimulants on B cell proliferation (certain lymphokines such as IL-5).…”

Section: Dextran Sulfate and Poly(ic)mentioning

confidence: 99%

Proliferative Assays for B Cell Function

Mond

Brunswick

2003

CP in Immunology

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This unit describes procedures for measuring the capacity of purified B cells to undergo proliferation. The method centers on the use of polyclonal stimulating agents (mitogens) because these agents stimulate the majority of B cells and because the alternative (measurement of antigen-induced proliferation) requires the laborious procedures of isolating antigen-specific B cells (which are otherwise present in too low a concentration in whole B cell populations). Cross-linking of the B cell antigen receptor, surface immunoglobulin (sIg), by specific antigen stimulates cells to proliferate prior to secreting Ig. For this purpose, monoclonal or heterologous affinity-purified anti-Ig antibodies are used. B cells can also be stimulated to proliferate by antigen-nonspecific reagents (mitogens), and it is also critical to study the role of these mitogens in B cell responses. Both of these systems have the advantage that the majority of B cells will be activated. The first basic protocol describes B cell proliferation induced by two commonly used stimulants--anti-Ig antibody (either anti-IgM or anti-IgD) and lipopolysaccharide (LPS)--as measured by incorporation of [3H]thymidine into dividing cells. Alternate protocols describe other commonly used mitogens as well as other means of measuring cell proliferation.

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Specific binding of poly(I) · poly(C) to the membrane of murine B lymphocyte subsets

Cited by 9 publications

References 9 publications

Preclinical Evaluation of the Effects of a Novel Antisense Compound Targeting C-rafKinase in Mice and Monkeys

Preclinical Evaluation of the Effects of a Novel Antisense Compound Targeting C-rafKinase in Mice and Monkeys

Cyclic AMP mediates the direct antiproliferative action of mismatched double-stranded RNA.

Proliferative Assays for B Cell Function

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