Interferon mediates Enhancement of Tumour Growth and Virus-induced Sarcomas in Mice

Gazdar, Adi F.; Sims, Harvie L.; Spahn, Gerard J.; Baron, Samuel

doi:10.1038/newbio245077a0

Cited by 7 publications

(5 citation statements)

References 14 publications

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“…For example, in the case of infection with an oncogenic virus, interferon produced in or near transformed cells could conceivably prevent (thymus-derived) T cells from destroying these cells, and favor their survival. In this respect it is pertinent to recall some experiments of Gazdar et al, showing that under certain well-defined conditions of timing and route of administration, interferon can favor tumor growth (33,34). On the other hand, if the infection takes place with a nontransforming virus, there may be some benefit in having at the site of infection a substance that actually limits cellmediated immune reactions.…”

Section: Effect Of Interferon Purified By Affinity Chromatographymentioning

confidence: 99%

Inhibition by interferon of delayed-type hypersensitivity in the mouse.

Maeyer¹,

Maeyer‐Guignard²,

Vandeputte³

1975

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

110

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The effect of interferon on delayed-type hypersensitivity to picryl chloride and sheep erythrocytes was examined in the mouse. When administered to sensitized animals on the day .before or the day of challenge, tissue culture interferon inhibited both the ear swelling induced by picryl chloride and footpad swelling induced by sheep erythrocytes. Newcastle disease virus, when injected into sensitized If-11 or If-14 congenic mice a few hours before challenge, caused an inhibition of delayedtype hypersensitivity which could be related to the amount of serum interferon induced by the virus. These results indicate that interferon production may represent one of the factors responsible for the depression of cell-mediated immune reactions during virus infection.The temporary decrease of cell-mediated immune reactions during virus infection is a well-known phenomenon, the mechanism of which has remained largely unexplained. The classic observation in this field was made in 1907 by von Pirquet, who described a decreased reactivity to the tuberculin skin test as a result of infection with measles virus; it has since been repeatedly confirmed and studied in great detail (1). Moreover, depression of tuberculin sensitivity in man also occurs after infection with varicella, influenza, and rubella virus, as well as after vaccination with measles, polio, yellow fever, and mumps virus (2-8). Similar effects have been reported in animals; for example, using skin allograft survival as a measure of cell-mediated immunity, Howard et al. showed that graft survival times were significantly prolonged in mice infected with lactic dehydrogenase virus shortly before or after grafting, and there are many other examples of immunodepression in animals after virus infection (9-11). One common denominator of all virus infections being the production of interferon, we have examined the possibility that interferon is capable of decreasing cell-mediated immune reactions in vivo. There were some good reasons for considering the role of interferon: the prolongation of skin allograft survival described in mice after administration of phytohemagglutinin or concanavalin A, two lectins that are also interferon inducers, and the fact that interferon has been shown to inhibit the proliferative phase of the one-way mixed lymphocyte reaction, which is considered by many to be an in vitro correlate of allograft rejection (12)(13)(14)(15)(16)(17). As a first model of cellmediated immunity, we have studied skin graft rejection in mice across an H-2 barrier, and a small but significant prolongation of graft survival after treatment of recipient mice with either interferon inducers or interferon preparations was observed (18,19). The effect of interferon preparations was independently confirmed by Hirsch et al. (20). In the present study, the effect of interferon on delayed-type hypersensitivity in mice was examined, using two different approaches:(1) interferon induction with Newcastle disease virus (NDV) in high-and low-interferon-producing congenic ...

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Section: Effect Of Interferon Purified By Affinity Chromatographymentioning

confidence: 99%

Inhibition by interferon of delayed-type hypersensitivity in the mouse.

Maeyer¹,

Maeyer‐Guignard²,

Vandeputte³

1975

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

110

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“…Interferon has been reported to enhance tumor incidence and size when it is administered prior to MSV, possibly owing to depression of the immu nologic response [28]. This situation cannot apply here because interferon, which could eventually have been synthesized in response to the viral infection, would distribute evenly throughout the body of te host irrespective of the location of the virus infection in relation to the site of the tumor.…”

Section: Discussionmentioning

confidence: 69%

Enhancement of Lewis Lung Carcinoma by the Concomitant Infection of the Host with Herpes simplex Virus Type 1 and Type 2

1983

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Infection with herpes simplex virus (HSV) enhances the growth of Lewis lung tumor (LLT). Infection with HSV-1 enhances as efficiently as HSV-2. A significant acceleration of primary tumor formation was obtained. In mice, lung metastases were increased in number and size above the controls. Enhancement occurred only with high doses of infectious virus and was also obtained only when the virus infection was at a site close to that of the tumor implantation. This finding, in addition to the lack of antigenicity of LLT, is interpreted as arguing against an immunologic mechanism of the phenomenon.

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“…Several investigators have shown that the development and progression of various virus-induced murine leukemias and sarcomas can be suppressed or delayed, provided that high doses of interferon are administered at frequent intervals (GRESSER et al a, b, c, d, 1968WHEELOCK and LARKE 1968;BERMAN 1970). The complexity of the effects of interferon in these model systems is illustrated by the findings that interferon inducers, and interferon itself under certain experimental conditions, can enhance growth of murine leukemias and sarcomas caused by type C RNA viruses (LARSON et al 1969;DECLERCQ and MERIGAN 1971;GAZDAR et al 1972GAZDAR et al , 1973. The complexity of the effects of interferon in these model systems is illustrated by the findings that interferon inducers, and interferon itself under certain experimental conditions, can enhance growth of murine leukemias and sarcomas caused by type C RNA viruses (LARSON et al 1969;DECLERCQ and MERIGAN 1971;GAZDAR et al 1972GAZDAR et al , 1973.…”

Section: Virus-induced Tumorsmentioning

confidence: 99%

Chemotherapy of Viral Infections

Jones¹

1982

Handbook of Experimental Pharmacology

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Interferon mediates Enhancement of Tumour Growth and Virus-induced Sarcomas in Mice

Cited by 7 publications

References 14 publications

Inhibition by interferon of delayed-type hypersensitivity in the mouse.

Inhibition by interferon of delayed-type hypersensitivity in the mouse.

Enhancement of Lewis Lung Carcinoma by the Concomitant Infection of the Host with Herpes simplex Virus Type 1 and Type 2

Chemotherapy of Viral Infections

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