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- Ankerst, Jaro, et al.
(author)
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Immunity to cancer. Naturally occurring tumours in domestic animals as models for research. Part 1
- 1973
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In: Bulletin of the World Health Organization. - 0042-9686. ; 49:1, s. 81-91
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Journal article (peer-reviewed)abstract
- PREVENTIVE VACCINATION IS SUCCESSFULLY PRACTISED TODAY AGAINST TWO NEOPLASTIC DISEASES OF DOMESTIC ANIMALS: fibropapillomatosis of cattle and Marek's disease of chickens (a lymphoproliferative disease). Also it may soon be possible to immunize cats against lymphosarcoma. This memorandum describes these diseases and the immunological reactions involved. It also mentions a number of other tumours that could be used for immunological studies.The greatest advances in immunity have been made with the tumours caused by viruses. The killed papillomavirus vaccine used against bovine papillomatosis produces demonstrable antibodies against the virus. In the case of Marek's disease of chickens, which is due to a herpesvirus, a live virus vaccine is used. This does not prevent infection with virulent virus, but prevents the development of neoplasia. The mechanism by which the vaccine produces its effect is not yet known. Immunization with live and with killed vaccines has been successfully carried out experimentally against leukosis of chickens, which is caused by an oncornavirus. There is evidence that it will be possible to vaccinate cats against lymphosarcoma with non-living vaccine.Naturally occurring cancer in domestic animals parallels cancer in man more closely than does experimentally induced cancer in inbred laboratory animals; therefore immunological studies with the former are more likely to yield results relevant to the problem in man. Experimental cancer in rodents provides models that have the great advantages of uniformity and availability, and they cannot be replaced. However, models in domestic animals offer valuable supplementary systems for research aimed at elucidating the basic principles of immunity to cancer.
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| 2. |
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| 5. |
- Ankerst, J., et al.
(author)
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Cytotoxicity induced by mixtures of adenovirus and specific antibodies - Induction of cytotoxic aggregates by homotypic anti-fibre sera and neutralization of the cytotoxicity by homotypic anti-hexon sera
- 1973
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In: Archiv für die gesamte Virusforschung. - 0003-9012. ; 41:1-2, s. 99-105
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Journal article (peer-reviewed)abstract
- Aggregates cytotoxie for human cells in vitro were produced when adenovirus type 5 was mixed with homotypic rabbit antiserum against whole virus particles at a certain restricted virus-antibody ratio. The same degree of cytotoxicity was obtained with mixtures of the virus and an antiserum against purified fibres of adenovirus type 5 at a certain proportion. The cytotoxicity could be neutralized by homotypic antisera against purified hexons. The sequence in which the two anti-capsomer sera were added to the virus was found to be of importance: complete neutralization of the cytotoxicity appeared when virus preparations were incubated with anti-hexon sera before cytotoxic aggregates were formed by antifibre sera. In this case even a significantly lower51Cr-release appeared than that produced by corresponding amounts of virus alone. No neutralization of the cytotoxicity was obtained when anti-hexon serum was added to the mixtures after formation of cytotoxic aggregates by anti-fibre antibodies.
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| 6. |
- Kjellen, L., et al.
(author)
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Cytotoxicity of adenovirus antibody aggregates : sensitivity to different cell strains, and inhibition by hexon antiserum and by complement
- 1973
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In: Journal of Virology. - : American Society for Microbiology. - 0022-538X .- 1098-5514. ; 12:1, s. 25-32
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Journal article (peer-reviewed)abstract
- Adenovirus antibody aggregates under defined conditions are cytotoxic in vitro. All members of adenovirus groups I, II, and III caused toxicity upon aggregation. The toxicity of the clusters is exerted by the virions. Toxicity is temperature dependent and may be caused by a mechanism similar to that used in viral penetration. Cells permitting direct viral penetration were all sensitive to the toxic aggregates. The toxicity seems to be related to hexon antigens on the surface of the virions since antihexon sera neutralized the toxicity. No evidence was obtained showing that pentons are required for this kind of cytotoxicity. Adenovirus types 3,5, and 9 were used in the experiment. Cytotoxicity was estimated by the 51Cr release assay. Complement factors could be excluded as mediators of the cytolytic reactions. Instead, complement was shown to prevent the formation of toxic aggregates or to neutralize the toxicity of preformed ones.
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| 7. |
- Kjellén, L., et al.
(author)
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Cytotoxicity of adenovirus‐antibody complexes. Specificity of antibody and virus‐antibody ratio at which cytotoxicity is induced
- 1973
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In: European Journal of Immunology. - : Wiley. - 0014-2980 .- 1521-4141. ; 3:2, s. 78-84
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Journal article (peer-reviewed)abstract
- Adenoviruses aggregate in the presence of type‐specific antibodies against whole virus particles. These aggregates were found to damage human cells in vitro in far higher order of magnitude than virus alone, when virus and type‐specific antibodies were mixed at a certain virus‐antibody ratio. No cytotoxicity occurred when the virus was mixed with type‐specific antibodies in higher or lower dilutions or when the virus was incubated with antisera against another adenovirus serotype. Furthermore, it was found that the cytotoxicity could be prevented by type‐specific anti‐hexon sera and that type‐specific anti‐fiber sera produced cytotoxic aggregates out of subtoxic ones. The presence of the cytotoxic aggregates was demonstrated by electron microscopy and by 51Cr release cytotoxicity tests.
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| 8. |
- Larsson, Inger, et al.
(author)
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Interferon production in glia and glioma cell lines
- 1978
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In: Infection and Immunity. - 1098-5522. ; 22:3, s. 786-789
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Journal article (peer-reviewed)abstract
- Interferon (IF) was produced in glia and glioma cell lines in titers comparable to those produced by human fibroblasts. It was inducible by both Sendai virus and polyriboinosinic:polyribocytidylic acid. "Superinduction" resulted in up to 500-fold-higher titers of IF. The IF appeared to be of the fibroblast type, as revealed by experiments using heat treatment, assay of antiviral activity in heterologous cell lines, and neutralization with specific antisera. Since large amounts of IF may easily be produced with glioma cell lines, such cells may be suitable for mass production of IF.
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| 9. |
- Lundgren, E, et al.
(author)
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Effects of leukocyte and fibroblast interferon on events in the fibroblast cell cycle
- 1979
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In: Journal of General Virology. - : Microbiology Society. - 1465-2099 .- 0022-1317. ; 42:3, s. 589-595
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Journal article (peer-reviewed)abstract
- Serum-depleted human foetal skin fibroblasts were stimulated by addition of 10% foetal calf serum to proliferate synchronously for at least one cell cycle. This proliferation was suppressed by leukocyte or fibroblast interferon (IF), which prolonged the G1 phase and diminished the rate of DNA synthesis during the S phase in a dose-dependent manner. When used in identical concentration, as judged in terms of units of antiviral activity, fibroblast IF had more pronounced effects on cell cycle events than leukocyte IF. Interferon exerted its effect in early G1, before the cells were irreversibly committed to DNA synthesis.
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| 10. |
- Miörner, Håkan, et al.
(author)
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Regulation of mitogen-induced lymphocyte DNA synthesis by human interferon of different origins
- 1978
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In: Cellular Immunology. - : Elsevier BV. - 0008-8749. ; 35:1, s. 15-24
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Journal article (peer-reviewed)abstract
- Human fibroblast and leukocyte interferons were found to suppress lymphocyte mitogenesis induced by optimal doses of phytohemagglutinin and concanavalin A. In certain situations (low doses of mitogen and/or low doses of interferon), however, interferon significantly enhanced mitogenesis. In experiments using varying concentrations of interferon, dose-response curves with different slopes were obtained for fibroblast and leukocyte interferons. The effect of interferon was apparently exerted during early stages of the lymphocyte cell cycle. There was no inhibitory effect of interferon if the lymphocytes were washed with medium before being exposed to mitogen. Interferon increased the binding of radiolabeled mitogens to cells. The results suggest that the immunological effects of interferon are consequences of actions on lymphoid cells. Fibroblast and leukocyte interferons seem to have different modes of action, or to bind differently to target cells. Possible mechanisms for the suppressive and enhancing effects of interferons on lymphoid cells are discussed.
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