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PubMed1992

Interferon-neutralizing or enhancing activities in hybridoma cell fluids after in vitro immunization.

Several hybridomas supernatants capable of interferon beta (IFN-beta) or "IFN epsilon" ("IFN-eps") neutralizing or enhancing activities were obtained after in vitro immunization of BALB/c and C57 mice spleen cells and their fusion with Sp2/0 plasmacytoma cells. Besides rather low anti-IFN-beta or "eps" antibody secretion several cloned hybridoma fluids contained a factor potentiating anti-viral activity of the both IFNs. It is speculated that this activity is due to production by some hybridomas of another lymphokine.

Animals↗
PubMed1992

Cytotoxicity of human beta-interferon produced in human glioma cells transfected with its gene by means of liposomes.

The cytotoxicity of human beta-interferon (HuIFN-beta) produced in human glioma cells was examined by use of our liposomes entrapping two plasmids, pSV2neo and pSVMTV-IFN-beta. After the cells had been transfected with these genes by means of the liposomes, neomycin-resistant cells were selected. When the selected cells were subjected to a single exposure to dexamethasone, all of the cells were found to produce HuIFN-beta and were eliminated by 8 days. Accordingly, the effect of HuIFN-beta produced in human glioma cells is considered to be cytocidal.

Cell Death↗
PubMedDate not supplied

Effect of natural beta-interferon on estrogen receptor mRNA of breast cancer cells.

We have demonstrated that natural beta-interferon (beta-IFN) enhances estrogen receptor (ER) mRNA of a human breast cancer cell line, CG-5. Cells were sensitive to the effect of beta-IFN at concentrations ranging from 10 to 100 IU/ml. The increase of ER mRNA was seen after 48 hr of treatment in at least three separate experiments. Our results are in agreement with the previously observed enhancement of receptor protein. In addition, they suggest that the IFN-induced promotion of the antiproliferative activity of drugs which act via ER may be due, in part, to increased receptor synthesis.

Blotting, Northern↗
PubMedDate not supplied

Ly-6A/E gene is widely expressed among transformed nonhematopoietic cells. Autocrine modulation by interferon.

Expression of the Ly-6A/E gene by transformed cells was investigated in 14 cell cultures of C57BL/6 and BALB/c mouse origin derived from spontaneous or chemically-induced non-hematopoietic tumours and from cells transformed by SV40 virus. Histologic types included carcinomas, sarcomas and a melanoma. Thirteen out of 14 cell cultures expressed membrane Ly-6A/E antigens; only the B16-A melanoma was negative, but it expressed Ly-6A/E after incubation with IFN-gamma. The effect of in vitro permanence was studied on early (< 10) and late (> 20) passages of B16-A melanoma and MN/MCA1 fibrosarcoma. Late passage B16-A cells were Ly-6A/E-negative and refractory to induction of Ly-6A/E (but not of H-2 antigens) by IFN-alpha, IFN-beta, or IFN-gamma; MN/MCA1 maintained a high expression of Ly-6A/E, but no increase was induced by IFNs. It was found that both early and late in vitro passages of MN/MCA1 actively produced IFN-alpha/beta. The analysis of cells of fibroblastic origin revealed a significant correlation between IFN release in the culture medium and Ly-6A/E levels. Culture of fibrosarcoma cells in the presence of an anti-IFN-alpha/beta serum reduced Ly-6A/E expression, thus indicating the existence of an autocrine loop.

Animals↗
PubMed1992

[Beta interferon therapy of HPV infections of the female genital tract].

The aim of the study was to evaluate the incidence of cervical and vaginal lesions due to Papilloma virus before and after beta-interferon therapy. Clinical symptoms and the therapeutic approach are described, whereas drug efficacy was assessed on a long-term basis. The study of 19 cases, brought to the Author's attention over an eight-year period (1984-91) confirms previously published reports: the use of interferon shows a good level of tolerability without complications and undeniable efficacy following surgical treatment.

Adult↗
PubMed1992

[Condylomata acuminata and associated infections--possibilities for therapy with interferon].

Recombinant alpha-Interferon can be used in primary therapy of condylomata acuminata. In our patients we found a response rate of 53%. Besides use in primary therapy the significant low rate of recurrences is important, thus offering the possibility of adjuvant interferon therapy after primary surgical treatment, where laser-vaporisation is best applied. Possible applications for primary and secondary treatment are shown. The rate of additional infections is of great importance; besides common agents for vaginal infections we found an elevated rate of HPV 16/18 with 47%.

Administration, Topical↗
PubMed1992

[Proteins induced by various types of double-stranded RNA and interferon type I in human fibroblasts. Correlation with antiviral activity of the substances].

Protein induction by new antiviral preparations of dsRNAs (larifan, ridostin, rifastin and poly(A).poly(U)) and recombinant beta-interferon in human fibroblasts (M19) was studied. The common gene products: 88, 80, 68, 58, 56, 52, 50 and 26 kD were detected in the spectra of the induced cytoplasmic polypeptides. At the same time the sets of the induced proteins had individual distinctions in various preparations. Induction of the 56-kD protein was more essential in the action of dsRNAs than that of interferon. The antiviral activity of dsRNAs and interferon preparations correlated with a relative increase in the synthesis of proteins with molecular weights of 88, 80 and 58 kD. The study results are in agreement with the fact that the dsRNAs have interferon-independent pathways of antiviral action with participation of 56- and 58-kD protein genes.

Antiviral Agents↗
PubMed1992

Effects of ultraviolet-inactivated feline leukemia virus on the production of alpha/beta interferon by feline peripheral blood mononuclear cells.

The effects of ultraviolet-inactivated feline leukemia virus (UV-FeLV) on the production of alpha and/or beta interferon (IFN) by mononuclear cells stimulated with the Newcastle disease virus (IFN-NDV) was investigated. The production of IFN-NDV and gamma IFN was suppressed by 50% as compared to the control in the presence of 200 ng/ml or 200 micrograms/ml of UV-FeLV, respectively. The presence of UV-FeLV decreased the rate of the production, but the time to reach the plateau of the IFN activity in the culture supernatant was not shortened in both IFNs. It was suggested that the suppressive effects of UV-FeLV against both IFNs were through rather similar mechanisms. The suppressive effects of UV-FeLV on IFN-NDV production was most evident in the cultures to which UV-FeLV was added at the early stages of the culture, and could not be demonstrated when UV-FeLV was added 8 hr after initiation of the culture. These data therefore indicate that non-infectious feline leukemia viral particles can modify the production of feline IFNs by peripheral blood mononuclear cells.

Animals↗
PubMed1992

Modulation of leukemic cell sensitivity to lymphokine-activated killer cytolysis: role of intercellular adhesion molecule-1.

The role of CD11/CD18 leukocyte adhesion molecules and their ligands in mediating non-major histocompatibility complex (MHC) restricted lymphocyte cytotoxicity is controversial. In order to examine the role of target cell intercellular adhesion molecule-1 (ICAM-1; CD54), a ligand of lymphocyte function-associated antigen (LFA-1) (CD11a/CD18), we exposed the human leukemia cell line, HL-60, to a variety of agents implicated in modulating ICAM-1 expression and/or sensitivity to lymphocyte cytolysis. Exposure of HL-60 cells to retinoic acid (RA), interferon (IFN)-alpha, IFN-beta, and IFN-gamma induced protection from lymphokine-activated killer (LAK) cytolysis. Only RA and IFN-gamma induced ICAM-1 expression. Tumor necrosis factor and vitamin D3, which also induced ICAM-1 expression, increased HL-60 sensitivity to LAK lysis. Granulocyte-macrophage colony-stimulating factor also increased sensitivity to LAK lysis; ICAM-1 was not induced. The state of cellular differentiation and expression of class I and II MHC antigens also did not correlate with sensitivity to LAK cytolysis. Exposure of untreated HL-60 cells and HL-60 cells expressing ICAM-1 to monoclonal antibody (mAb) versus ICAM-1 did not modulate LAK sensitivity. Exposure of LAK cells to mAb versus LFA-1 partially inhibited cytolysis; mAb versus CD18 inhibited cytolysis more completely. HL-60 cells were resistant to natural killer lysis; exposure to the various experimental agents did not alter sensitivity. We conclude that leukemic cell sensitivity to LAK cytolysis can be modulated by a variety of agents. Although our results suggest a role for leukocyte CD11/CD18 adhesion molecules in LAK cytolysis, the poor correlation between ICAM-1 expression and sensitivity to LAK lysis suggest that interactions other than LFA-1/ICAM-1 conjugation may be more central to the processes involved.

Antibodies, Monoclonal↗
PubMed1992

Synergistic antitumor interactions between newly synthesized ruthenium complexes and cytokines in human colon carcinoma cell lines.

The purpose of these studies was to assess the antiproliferative properties of newly synthesized, heterocyclic ruthenium complexes alone and in combination with cytokines (tumor necrosis factor-alpha, interferon alfa, beta, and gamma) against various human colon carcinoma cell lines. To determine whether any of these ruthenium compounds possesses antitumor activity and reveals synergistic interaction with cytokines six new ruthenium complexes were studied. All six compounds exerted dose-dependent antitumor effects in all colon cancer cell lines tested. The most effective compounds were trans-indazolium[tetrachloro(2H-indazole)ruthenate (III, N1)] and trans-indazolium[tetrachlorobis(1 H-indazole)ruthenate (III, N2)]. Interferon alfa, beta, and gamma as well as tumor necrosis factor-alpha exerted only minimal antiproliferative effects in colon carcinoma cell lines. The data were further analyzed to determine whether preincubation with cytokines altered sensitivity of the cells to synergistically potentiating growth-inhibitory effects. Although simultaneous incubation of ruthenium complexes and interferon did not result in synergistic or additive interactions, 24-hour preincubation with interferon alfa, beta, and gamma significantly enhanced antitumor activity. We conclude from these data that two of six newly synthesized ruthenium complexes possess antiproliferative activity against a panel of human colon carcinoma cell lines. Moreover, biological modulation with interferon using 24-hour preincubation resulted in synergistic interactions. We are planning a phase I trial, since antitumor activity of these ruthenium compounds has been demonstrated in vitro and in vivo, and toxicity as well as stability data are now available.

Carcinoma↗
PubMed1992

The clinical application of the interferons: a review. NSW Therapeutic Assessment Group.

OBJECTIVES: To review the clinical information on the use of alpha, beta and gamma interferons and to classify the use of alpha interferons in Australia according to approved indications, indications for which there is good supporting evidence and indications where therapy is under investigation; and to estimate the cost of therapy with alpha interferons in New South Wales in 1991. DATA SOURCES: Data were obtained from computerised literature searches. DATA EXTRACTION: A position paper was drafted on behalf of the NSW Therapeutic Assessment Group (NSWTAG). This was circulated to clinicians identified as having a particular interest in the use of the interferons in major NSW teaching hospitals, for comment and amendment where necessary. CONCLUSIONS: Two forms of alpha interferon, interferon alfa-2b and interferon alfa-2a have been approved for use in Australia, interferon alfa-2b for use in the management of hairy cell leukaemia and condylomata acuminata and interferon alfa-2a for use in the management of hairy cell leukaemia and human immunodeficiency virus (HIV) related Kaposi's sarcoma. Applications have been lodged for the use of interferon alfa-2b in HIV related Kaposi's sarcoma, cutaneous basal cell carcinoma and hepatitis B and C and for the use of interferon alfa-2a in the management of hepatitis B, cutaneous T-cell lymphoma and metastatic renal cancer. Interferon alfa-n1 is not available in Australia except for use in a clinical trial in patients who are HIV seropositive. The use of the alpha interferons is currently under investigation in a wide variety of other diseases, with the likelihood that other indications will soon be established. However, the alpha interferons are generally not regarded as first line agents. Beta and gamma interferons have been studied less intensively than the alpha interferons, but it is likely that selected applications for their use will also be defined with the passage of time.

Australia↗
PubMed1992

[Role of interferon in the treatment of renal cancer in adults].

Alpha interferon is effective in the treatment of metastatic renal cell cancer. To obtain a maximal efficacy, alpha interferon should be used at a dose of 10 MU/m2, or 18 MU total dose, given daily or three times a week. At such doses interferon produces flu-like symptoms and severe asthenia and thus should be proposed only to patients who have a good performance status. The response rate is low, in the order of 15-20%, and the median remission duration is short (6-10 months). However a few patients experience very durable remissions, sometimes for more than 5 years. The response rate may possibly be improved to 20% to 35% by combining interferon alpha with antineoplastic agents or to other cytokines, namely interleukin 2. Finally because of its supposed mechanisms of action-direct tumor growth inhibition and enhancement of the host's immune defenses--interferon may be of benefit in the adjuvant setting.

Adult↗
PubMed1992

Elevated interleukin-6 and gamma-globulin during interferon therapy of hepatitis B.

A 49-yr-old man with chronic hepatitis B manifested hypergammaglobulinemia, lymphadenopathy, and a high serum interleukin-6 level following treatment with recombinant human alpha-interferon. One month later, when the patient was treated with natural beta-interferon, serum levels of interleukin-6 and gamma-globulin increased again. The serum gamma-globulin decreased to the pretreatment level after discontinuation of interferon therapy. The serum alanine aminotransferase level remained normal for 6 months. In this case, hypergammaglobulinemia and lymphadenopathy, as well as the elevated serum interleukin-6 level, were considered to be signs of highly enhanced humoral immunity related to alpha- and beta-interferon therapy.

Alanine Transaminase↗
PubMedDate not supplied

Natural killer cell activity against cultured melanoma cells: a dye-reduction technique with studies on augmented activity by interferon subtypes.

We assessed natural killer (NK) cell activity against cultured melanoma cells using a novel method, with observations on the comparative effects of interferons (IFNs) in NK-stimulating and anti-proliferative assays. Since the tumour cells tested were adherent, a semi-automated colorimetric MTT dye reduction assay was developed to assess NK activity. The three adherent human melanoma cell lines Sk-Mel-28, MM418 and MM96 were shown to be suitable targets for determining NK activity. Also, these were representative of the range of sensitivities of melanoma cells to the anti-proliferative action of type 1 IFNs. The dose-dependent stimulation of NK activity by type 1 IFNs was confirmed in this alternative assay system. IFN-alpha 2b and IFN-beta ser had equivalent stimulatory activities, and IFN-alpha 4 proved less effective, as with assays using the classical K562 system. Augmented NK cytotoxicity did not correlate with anti-proliferative effects of IFN. In anti-proliferative assays, the hierarchy of activity is IFN-beta greater than IFN-alpha 2 greater than IFN-alpha 4, whereas, in the NK augmentation assay IFN-beta and IFN-alpha 2 were of equivalent activity. Interestingly, MM96 was the cell line most resistant to the direct anti-proliferative action of IFN, yet it was the most susceptible of the melanoma cell lines to cytotoxicity by NK cells, whether stimulated or unstimulated by IFN.

Cytotoxicity, Immunologic↗
PubMed1992

Correlation between interferon (IFN) alpha resistance and deletion of the IFN alpha/beta genes in acute leukemia cell lines suggests selection against the IFN system.

Homozygous and hemizygous deletions of the interferon A (IFNA) and IFNB genes have been frequently observed in acute leukemia cell lines, primary acute leukemia cases, and gliomas. Because IFNs have an antiproliferative effect, selection against the IFN alpha/beta system could play a role or accompany the development of the malignant phenotype. Although the deletion of the IFNA/B genes could interrupt an autocrine loop that controls cell proliferation, cells would still respond to exogenous IFN alpha/beta and, thus, lesions at the receptor or signal transduction level should also be present to render cells resistant to exogenous IFN alpha/beta. To test if selection against the IFN system was operating in acute leukemias, the sensitivity to the antiproliferative effect of IFN alpha 2 was studied in acute leukemia cell lines with and without alterations of the IFNA/B genes. We found that 10 of 11 acute leukemia cell lines with alterations of the IFNA/B genes were resistant to the antiproliferative effect of IFN alpha 2, whereas only two of eight cell lines with normal IFNA/B genes were IFN-resistant. We then examined the possibility that an alteration of the receptor expression could account for the lack of response to IFN alpha 2. No significant alteration in the expression or structure of the IFN alpha receptor was observed. We also studied the downmodulation of the alpha subunit of the IFN alpha receptor upon IFN alpha 2 binding. One cell line with deletion of the IFNA/B genes showed impaired downmodulation of the IFN alpha receptor. The data presented here suggest that selection against the IFN alpha/beta system could play a role or accompany the development of the malignant phenotype.

Acute Disease↗
PubMedDate not supplied

The effects of interferon-alpha/beta in a model of rat heart transplantation.

Interferons have multiple immunologic effects. One such effect is the activation of expression of cell surface antigens. Interferon alpha/beta enhance expression of class I but not class II histocompatibility antigens. Contradictory information has been published regarding the effect of interferon-alpha/beta administration in patients with kidney transplantation. In a model of rat heart transplantation we demonstrated that administration of interferon-alpha/beta accelerated rejection in a dose-dependent fashion in the absence of maintenance cyclosporine. Animals treated with maintenance cyclosporine had evidence of increased rejection at 20 days that was resolved completely at 45 days with cyclosporine alone.

Animals↗