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Biomedical subjects

F Dianzani

Publications and source records attributed to F Dianzani.

At least 145 records · Page 8Linked to original sources
PubMed1980

Immune and virus-induced interferons may activate cells by different derepressional mechanisms.

Virus-induced interferon (VIF), and immune interferon (IIF) produced by lymphocytes following activation by various mitogens (phytohaemagglutinin, concanavalin A, staphlococcal enterotoxin A) or by specific antigenic stimulation (tuberculin, bacterial toxoids, and viral antigens) show important functional differences. These include different antitumour and immunoregulatory activities and differential inhibition of activity by mercaptoethanol. Another important difference has recently been shown: cells treated with IIF acquire the antiviral state much more slowly than those treated with VIF. This may be due to (1) difference in cellular receptors, (2) presence of an inhibitor of antiviral activity in the IIF preparations, or (3) a different mechanism of activation of the antiviral state by the two types of interferon. The first two hypotheses seem unlikely, since (1) no difference between cell association by the two types of interferon has been detected, and (2) the presence of the slow acting IIF preparation did not inhibit the rapid activation by VIF. The present study shows that the different kinetics of induction of the antiviral state result from a major difference in the mechanism by which IIF and VIF activate cells.

Animals↗
PubMed1980

Human immune interferon: induction in lymphoid cells by a calcium ionophore.

Human lymphocyte cultures produced interferon after treatment with the calcium ionophore A23187, but not after treatment with potassium ionophore nonactin. Interferon production was detectable between 3 and 6 h after ionophore treatment and reached the maximum level between 12 and 24 h. Ionophore-induced interferon appeared to be immune interferon on the basis of acid lability, lack of neutralization by antibody to leukocyte interferon, slow kinetics of activation of the antiviral state, and molecular characterization by isoelectrofocusing.

Adult↗
PubMed1979

Large-scale production and physicochemical characterization of human immune interferon.

Large-scale production of crude high-titered (10(2.3) to 10(4) U/ml) human immune interferon (type II) was carried out in roller bottle cultures of human peripheral lymphocytes by using the T-cell mitogen staphylococcal enterotoxin A. Over 99% of human immune interferon was destroyed by pH 2 or heat at 56 degrees C for 1 h. The interferon was not neutralized by antibody to human leukocyte interferon. The kinetics of development of the antiviral state were slow for immune interferon relative to those for leukocyte interferon. Ultrogel AcA 54 chromatography of crude or the concentrated interferon resulted in two peaks of activity, a major one (87% of recovered activity) with a molecular weight of 40,000 to 46,000 and a minor peak of molecular weight 65,000 to 70,000. The column elution buffer consisting of 18% ethylene glycol and 1 M NaCl in phosphate-buffered saline resulted in at least 100% recovery of added interferon. The data suggest, then, that the interferon produced under large-scale conditions was immune (type II). The efficiency of the production was comparable to that described for large-scale production of human leukocyte interferon. Our large-scale production system for human immune interferon offers a feasible approach to preparation of large quantities of purified immune interferon for structure studies, antibody production, and clinical application.

Cell Line↗
PubMed1979

Enzymatic induction of interferon production by galactose oxidase treatment of human lymphoid cells.

Human lymphocyte cultures produced large amounts of interferon after treatment with the enzyme galactose oxidase. Interferon production was detectable as early as 3 h after enzymatic treatment and reached a level of about 10(4) reference units 20 to 24 h later. Galactose oxidase-induced interferon appeared to be immune interferon on the basis of acid lability, lack of neutralization by antibody to leukocyte interferon, and slow kinetics of activation of the cellular antiviral state. Interferon production was inhibited to the same extent (99%) by pretreatment of the cells with beta-galactosidase or with neuraminidase followed by beta-galactosidase, suggesting that the critical event for activation of interferon production is the oxidation of exposed galactose residues on lymphocyte membrane.

DNA↗
PubMed1979

Induction of an inhibitor of interferon action in a mouse lymphokine preparation.

An inhibitor of interferon action was identified in mouse lymphokine preparations. The inhibito was first detected in the supernatant fluid of mouse spleen cells at 72 h after stimulation by staphylococcal enterotoxin A. Inhibitor was not detected in supernatant fluids from unstimulated cultures. This inhibitor blocks the antiviral activity of both immune and fibroblast interferons. The inhibitor was purified 1,000-fold by two-step column chromatography. The partially purified inhibitor blocked the antiviral activity of up to 400 U of interferon. The immunosuppressive effect of interferon was also blocked by the inhibitor, suggesting that the inhibitor may modulate the immunoregulatory function of interferon.

Animals↗
PubMed1978

Rapid activation of the interferon system in vivo.

Experiments were carried out to study the kinetics of local interferon production in the subcutaneous tissues of rats stimulated with Newcastle disease virus. Specifically, the interferon produced and released in the extracellular fluids was collected at various intervals of time in micropore chambers implanted into the subcutaneous tissue of rats. Interferon was detected at moderate titers 1 h after induction, and it was present at high titer at 2 h. The interferon levels remained remarkably high in the samples collected after 3, 5, and 24 h, and in some rats it was still detectable after 48 and 72 h. Since control experiments showed that it requires 2 to 3 h for interferon to penetrate the chambers, it may be concluded that high concentrations of interferon are present in the extracellular fluid within 1 h of induction. The evaluation of the kinetics of production and of the concentrations attained in the extracellular fluid suggests that in a solid tissue a cell infected by a potent interferon inducer may produce interferon early enough and in sufficient quantity to protect neighboring cells before the production of progeny virions.

Animals↗
PubMed1977

Effect of anti-mu-chain-specific immunosuppression on Chikungunya virus encephalitis of mice.

Mice neonatally immunosuppressed with anti-mu antiserum failed to produce circulating antibodies to sheep erythrocytes and showed a marked decrease in circulating immunoglobulins. However, when they were intracerebrally infected with Chikungunya virus (a group A togavirus), they showed a mortality rate consistently lower than non-immunosuppressed control mice. Several possible explanations for this finding are discussed.

Animals↗