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At least 613 records · Page 34Linked to original sources
PubMed1985

Effects of cimetidine on various biological activities of human leucocyte interferon and on interferon production in lymphocytes.

In vitro effects of cimetidine on the antiviral, the antiproliferative and the natural killer (NK) cell stimulating activities of human leucocyte interferon (IFN-alpha (Le], and on the Sendai virus induced interferon production in lymphocytes were investigated. The antiviral activity of IFN-alpha (Le) was dosedependently enhanced by cimetidine, which alone did not demonstrate any antiviral action. The observed titer of the same IFN preparation titrated with 60 micrograms/ml of cimetidine was significantly higher (p less than 0.05) than that without cimetidine. Cimetidine slightly but dosedependently inhibited the growth of Daudi or G-361 cells. The combination effects of these two agents were revealed to be statistically additive or synergistic. The NK cell activity of peripheral blood lymphocytes (PBL) was suppressed after a 16 hr pretreatment with cimetidine. Furthermore, the interferon production in normal lymphocyte cultures was suppressed dosedependently by cimetidine. On the other hand, the augmentation of the NK cell activity by interferon was further potentiated by cimetidine.

Cell Division↗
PubMed1997

Cutaneous necrosis associated with recombinant interferon injection. Report of three cases with interferon beta-1b and review of the literature.

Interferons are cytokines produced by cells in response to stimulation by certain antigens and infectious agents. In recent years, recombinant interferons have been developed, which have antiviral, antiproliferative, and immunomodulatory functions. Several cutaneous reactions have been reported, including cutaneous ulceration at injection sites. We now report three cases of cutaneous ulceration caused by interferon beta-1b injections. In addition, we review all of the previously reported cases of cutaneous ulceration caused by recombinant interferons and discuss the different mechanisms by which these substances may produce this effect.

Adjuvants, Immunologic↗
PubMedDate not supplied

Antiviral effects of highly purified bacteria-derived human leukocyte interferons (subtypes A and D) and a human fibroblast interferon against herpes virus infection of the rabbit eye.

Highly purified preparations of two recombinant-DNA derived human leukocyte interferon subtypes (LeIF-A and LeIF-D) and a similarly derived fibroblast interferon were compared for efficacy against herpes simplex virus, type 1, infection of the rabbit cornea. LeIF-D appeared to be more effective than LeIF-A especially when compared on the basis of interferon units. The fibroblast interferon showed no significant effects. The greater activity of LeIF-D compared with LeIF-A could be due to greater direct antiviral effects, as observed in rabbit cell cultures.

Animals↗
PubMed1985

The physiological interferon response: IV. Production of interferon by the perfused human placenta at term.

Human placentas at term, free of bacterial and viral diseases, have been perfused and maintained sterile for up to 13 hr. Several parameters indicate that the organs remained viable and released interferon into the perfusate in a progressive fashion. The amount of interferon was small and the individual variations indicate that there are "poor" and "good" placenta producers. Both interferons -alpha and -beta were produced with a prevalence of the latter type. The partial acid lability and the type heterogeneity suggest that under physiological conditions the placentas produce unusual interferons, the function of which remains speculative.

Amnion↗
PubMedDate not supplied

[Liposome-incorporated interferon. The design of liposomal interferon].

To develop bound interferon, purified phospholipids (PL), obtained from waste products of soy-bean oil production, were chosen as lipid carries. The method for the development of the liposomal interferon complex was proposed. As shown in this study, with regard to the composition of the most significant PL fractions the carrier obtained from waste products of soy-bean processing proved to be more acceptable for humans than egg-yolk PL, traditionally used in practical liposomology. The advantage of the purified concentrate of waste products of soy-bean oil production was its greater affinity with the PL fraction profile of human internal organs (the liver, the kidneys) than the composition of PL of animal origin. The dispersion and stability of interferon-containing liposomes was evaluated. The interferon incorporation coefficient of soy-bean PL proved to exceed that of egg-yolk PL.

Animals↗
PubMedDate not supplied

[Characteristics of messenger RNA for interferon and of interferon-inducing RNA isolated from Newcastle disease virus infected cells].

Two kinds of RNA capable of producing interferon in a heterologous cell system occur in the cells producing interferon in response to induction by Newcastle disease virus. One of them has messenger activity for interferon and is presented by a single-stranded structure with sedimentation constant of 10-22 S. This RNA appears to belong to cellular messenger RNA. The other is capable of inducing interferon production by heterogenous cells, resistant to treatment with RN-ase and has sedimentation constant greater than 35 S. In our opinion, this RNA is the primary replicative RNA of the virus-inducer.

Culture Techniques↗
PubMed1985

[Interferon-inducing and antiviral effects of inosiplex in combination with high-molecular interferon inducers].

It has been shown that the immunostimulant inosiplex (IP) is capable of inducing interferon production in mice and of stimulating interferon induction by high-molecular inducers. The combined use of IP and poly (G)-poly (C) or dsRNA (RFf2) leads to a longer interferon circulation in the blood. All the combination schemes ensuring the effect of interferon production prolongation were tested for anti-viral activity. The prophylactic administration of the drugs permitted the attainment in mice of the increased resistance to experimental influenza.

Animals↗
PubMedDate not supplied

Regulation of natural killer cytotoxicity by recombinant alpha interferons. Augmentation by IFN-alpha 7, an interferon similar to IFN-alpha J.

The structure-function relationship of several recombinant human alpha interferons (IFN-alpha) (IFN-alpha 1, IFN-alpha 2, IFN-alpha 4, IFN-alpha 7, IFN-alpha 2/alpha 1 and IFN-delta 4 alpha 1) was investigated with respect to their ability to augment natural killer (NK) cytotoxicity of human peripheral blood mononuclear cells (PBMC) against hemopoietic tumor cell lines. Although all these IFNs significantly augmented NK cytotoxicity against the K562, Daudi and U937 targets, significant quantitave differences were observed in their ability to augment NK. INF-alpha 4, IFN-alpha 2 and IFN-alpha 2/alpha 1 were able to augment NK at low concentrations (less than 0.1 ng/ml), whereas IFN-alpha 7, IFN-alpha 1 and IFN-delta 4 alpha 1 required significantly higher concentrations (3 ng/ml or higher). The cumulative rank order of INFs on the basis of NK augmenting ability was found to be: IFN-alpha 4 approximately IFN-alpha 2 approximately IFN-alpha 2/alpha 1 greater than IFN-alpha 7 greater than IFN-alpha 1 approximately IFN-delta 4 alpha 1. To determine synergism or potentiation in the ability of IFNs to augment NK cytotoxicity, we investigated the effect of simultaneous, sequential and reversed order of treatment of human PBMC by these IFNs. Such potentiation or synergism was not observed. In addition, all these IFNs were able to augment NK cytotoxicity against targets from malignant melanoma cell lines. IFN-alpha 7 augmented regularly and reproducibly NK cytotoxicity in 15 of 19 normal donors examined (79%). This augmentation was blocked by an anti-IFN-alpha antibody. Concentrations of IFN-alpha 7 as low as 0.06 ng/ml were able significantly to augment NK cytotoxicity of PBMC after incubation for one hour at 37 degrees C. In contrast to these findings, IFN-alpha J, an interferon similar to IFN-alpha 7, has been report to be incapable of augmenting NK cytotoxicity and also of interfering with augmentation of NK by other IFNs. Sequential treatment of PBMC first with IFN-alpha 7 and then with other interferons did not prevent the augmentation of NK. Similarly, simultaneous treatment with IFN-alpha 7 and other interferons did not prevent augmentation of NK. In both treatments IFN-alpha J has been reported to prevent augmentation of NK. IFN alpha J and IFN-alpha 7 differ only by one amino acid, at position 107, where a lysine in IFN-alpha J has been replaced by a glutamic acid in the IFN-alpha 7.(ABSTRACT TRUNCATED AT 250 WORDS)

Amino Acid Sequence↗
PubMed1987

[Phase II study of recombinant human interferon gamma (S-6810) in renal cell carcinoma. Urological Cooperative Study Group of Recombinant Human Interferon Gamma (S-6810)].

A phase II study of recombinant human interferon gamma (rHuIFN-gamma) administered intravenously and intramuscularly was carried out in 84 patients with advanced renal cell carcinoma with the cooperation of 18 institutions throughout Japan. The eligibility of the patients and evaluation of the responses were undertaken according to the general criteria proposed by Drs. Koyama and Saito. Out of 84 cases entered in this phase II study, 62 patients were evaluable for antitumor effects. In the case of continuous administration of 8-12 X 10(6) U/m2/day interferon for 4 weeks, 32 patients were evaluable. The response rate was 6.3%. In the case of intermittent therapy of 40 X 10(6) U/m2/day interferon for 8 weeks, six out of 30 patients (20%) were evaluable as responders. Among them, one patient showed a complete response, all patients tolerated this type of interferon well. Major adverse effects were fever (86.8%), anorexia (67.1%), fatigue (53.9%) and leukopenia (42.1%). No life-threatening toxicities were found. The results of this study showed that rHuIFN-gamma had antitumor activity against renal cell carcinoma.

Adult↗
PubMed1977

Molecular mechanisms of the antiviral action of interferon: effects of interferon on the transcription of viral messenger RNA.

Evidence from a number of virus-cell systems, discussed above and in other papers in this section, shows that the resistance to virus infection induced by interferon is characterized by inhibition of both primary transcription and translation. This may be because interferon induces two (or more) distinct "antiviral proteins" which inhibit, respectively, the transcription and the translation of virus genetic information. Although both may be present in interferon treated cells, the one which is manifest in any given experimental system may depend on whether transcription or translation is the primary event in the replication of the particular virus, and upon the accessibility of the viral nucleic acid. Alternatively, inhibition of transcription and translation may be mediated by a single antiviral protein which is able to distinguish viral from cellular nucleotide sequences in both DNA and RNA. The interferon-induced ribosome-associated inhibitors of viral mRNA translation (see related papers in this section) are prime candidates for such an antiviral protein.

DNA Viruses↗
PubMed1987

Interferons as gene activators. Characteristics of an interferon-activatable enhancer.

Previously we linked a 0.8-kilobase segment (including the 5'-flanking region and the 5'-terminal exon) of an interferon-activatable mouse gene (202 gene) to the chloramphenicol acetyltransferase gene and transfected the construct into mouse Ltk- cells (Samanta, H., Engel, D. A., Chao, H. M., Thakur, A., Garcia-Blanco, M. A., and Lengyel, P. (1986) J. Biol. Chem. 261, 11849-11858). Treatment of these cells with mouse beta-interferon increased the expression of the chloramphenicol acetyltransferase gene 5-10-fold. Here we demonstrate that this segment from the 202 gene has characteristics of an interferon-activatable enhancer: (a) it can activate a heterologous promoter (SV40 early promoter), (b) it is active in both the appropriate and the inverted orientation and in either upstream or downstream locations from the promoter activated, and (c) treatment of cells with interferon increases its activity severalfold.

Animals↗
PubMed1985

Interferon-like activity in an anti-interferon anti-idiotypic hybridoma antibody.

We describe here an anti-idiotypic hybridoma antibody directed against affinity-purified rabbit idiotypic antibodies (Rb-Id) to a homogeneous protein, the recombinant human leukocyte A interferon (rIFN-alpha A). The supernatant of the hybridoma, designated 3-1B, was able to inhibit the neutralization of rIFN-alpha A activity by the idiotypic antibodies. An in vivo passage of uncloned 3-1B cells yielded hybridoma cells (presumably a subclone), designated 3B1, the supernatant of which exhibited interferon-like antiviral activity with both bovine kidney (MDBK) cells and human amnion (WISH) cells. This activity could be absorbed by polymer-bound goat anti-mouse immunoglobulin serum and by Rb-Id coupled to Affi-Gel 10, and could be partially eluted from the latter at pH 2.5. The anti-idiotypic hybridoma antibody was able to compete with 125I-rIFN-alpha A for binding to the Rb-Id and also to interferon receptor-bearing MDBK cells. The clinical significance of an interferon-like anti-idiotypic antibody is discussed.

Absorption↗
PubMed1976

Interferon-producing capacity of human tonsil cells and properties of interferon produced by these cells.

Tonsils excised from human beings for chronic tonsillitis have been shown to be an accessible and sufficiently rich source of human lymphocytes. Tonsil cells produced interferon as intensively as blood leukocytes and the properties of this interferon were similar to those of leukocyte interferon. The optimal conditions for interferon production by tonsil cells were established.

Adenoviridae↗
PubMed1980

Activation of 2',5'-oligo(A) polymerase and protein kinase of interferon-treated HeLa cells by 2'-O-methylated poly (inosinic acid) . poly(cytidylic acid), Correlations with interferon-inducing activity.

An oligonucleotide polymerase and a protein kinase which require double-stranded RNA (dsRNA) for activation are induced in HeLa cells by human fibroblast interferon. The polymerase synthesizes a series of oligonucleotides from ATP, whereas the kinase phosphorylates a polypeptide of Mr = 72,000 and the alpha subunit of initiation factor eIF-2. Partially or fully 2'-O-methylated derivatives of poly(inosinic acid) . poly(cytidylic acid) (rIn . rCn) were used to determine the structural requirements of dsRNA in the activation of these two enzymes. While fully methylated polymers failed to activate either enzyme, partially methylated polymers activated the enzymes in specific manners. The activation of the kinase by the rIn . rCn analogues was affected more severely by the level of methylation than was the activation of the polymerase. Moreover, fully methylated analogues blocked the activation of the kinase by rIn . rCn but not the activation of the polymerase. These observations are consistent with a biphasic model for enzyme activation similar to that proposed for interferon induction, which required the recognition of a relatively small region of rIn . rCn as the last step. Differences in the activation of the polymerase and kinase are explicable on the basis of the polymerase requirement for a smaller recognition region of the rIn . rCn duplex than the kinase. Dependence of polymerase activation on the level of methylation shows striking similarities with the interferon inducing activities of these analogues, suggesting a possible relationship between polymerase activation and interferon induction.

2',5'-Oligoadenylate Synthetase↗
PubMed1980

Extracorporeal interferon therapy in malignant melanoma. Significant economies of interferon in an extracorporeal chamber.

A new method is described for interferon therapy. The procedure involves immobilization of interferon with maintained activity to the surfaces of an extracorporeal perfusion chamber made from polymethylmethacrylate, having a surface area of 0.5 m2 and housing 150 ml blood. The interferon activity remains for at least 3 weeks in a chamber used in patients. Three cases of malignant melanoma, stage II, were treated for 35 to 50 h. The treatment induced increased natural killer activity against melanoma target cells (cytotoxicity index +45--65%) which lasted even after cessation of therapy. the drastic reduction in costs for this type of interferon therapy is underlined.

Costs and Cost Analysis↗
PubMed1984

Influence of thymic hormones on mitogen-induced interferon production in lymphocytes. II. Enhancement of Con-A-induced immune interferon production by a synthetic thymopoietin pentapeptide.

A synthetic thymic pentapeptide was used for prestimulation of mouse lymphocytes in vivo. This pentapeptide (DAc- Glu3 -TP5) affected the cAMP and cGMP levels positively and decreased the 3H-thymidine incorporation in lymphocyte cultures significantly. In combination with Con A DAc- Glu3 -TP5 influenced the production of interferon. After in vivo pretreatment of adult hybrid mice with DAc- Glu3 -TP5 the mitogen-induced interferon production was 3 to 7 times higher than in controls. The interferon produced was immune interferon (IFN gamma) as determined by pH 2-sensitivity and lack of neutralization by mouse IFN beta-antibodies.

Animals↗
PubMed1978

Role of interferon in the pathogenesis of viral diseases of mice as demonstrated by the use of anti-interferon serum. V. Protective role in mouse hepatitis virus type 3 infection of susceptible and resistant strains of mice.

Potent sheep anti-mouse interferon globulin has been used to determine the role of virus-induced interferon in mouse hepatitis virus type 3-infected susceptible (C57BL/6), semiresistant (C3H/He), and resistant (A/J) strains of mice. Injection of anti-interferon globulin accelerated the onset of death in C57BL/6 mice, induced almost 100% mortality in C3H/He mice that usually do not die of acute disease, and caused death in 4- and 6-week-old A/J mice, but not in older mice. We conclude that interferon is an important host defense factor in the initial response of different strains of mice to MHV-3 infection. Other factors, however, such as the capacity of macrophages to restrict viral multiplication probably underlie the genetically determined susceptibility or resistance of mice to MHV-3 infection.

Animals↗