Murine sarcoma virus (msv)‐induced tumors in mice. I. Distribution of msv‐immune cytolytic t lymphocytes <i>in vivo</i>

Plata, Fernando; Sordat, Bernard

doi:10.1002/ijc.2910190210

Cited by 30 publications

(20 citation statements)

References 25 publications

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“…Similarly the carcinomas of the cervix uteri, skin and lip may be linked to papilloma viruses [46]. Virally transformed cells may be strongly antigenic [33,41,71]. It is reasonable to assume that these antigenic tumour cells can cause an immune reaction that induces CTLs which kill these virally induced tumour cells in the healthy person.…”

Section: Resistance Against Spontaneously De Novo Arising Tumour Cellsmentioning

confidence: 99%

Immune surveillance and natural resistance: an evaluation

Otter

1986

Cancer Immunol Immunother

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Concepts in tumour immunology are changing fundamentally. Around 1970 tumour immunology contained the following related concepts: Thousands of tumour cells arise de novo each day. Tumour cells are antigenic in their host. All these antigenic tumour cells are killed by a strong immune surveillance system. A more likely set of concepts looks as follows: Tumour cells do not arise frequently. Tumour cells may be antigenic or not. There is no need to postulate a very strong immune surveillance or natural resistance system. In this paper I am reviewing our present knowledge of immune surveillance and natural resistance. Only scanty information appears to be available. This information suggests that virally induced tumours are usually killed by cytotoxic T lymphocytes, and natural killer cells, whereas immune surveillance and natural resistance against other tumours may be quite weak.

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Section: Resistance Against Spontaneously De Novo Arising Tumour Cellsmentioning

confidence: 99%

Immune surveillance and natural resistance: an evaluation

Otter

1986

Cancer Immunol Immunother

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“…Cytotoxic activity associated with spleen cells from animals undergoing regression of an autochthonous or a syngeneic tumor as well as those immunized with syngeneic tumors is often not detectable, or very low if detected [4,6,8,9,14,15,20]. Nevertheless substantial cytotoxic activities are often developed at the site of the regressing tumor or of tumor immunization [4,8,14,20].…”

Section: Introductionmentioning

confidence: 99%

Augmented induction of antitumor cells in vivo by cyclophosphamide fails to benefit antitumor resistance of the host

Ryoyama

1989

Cancer Immunol Immunother

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The present study was designed to examine whether cyclophosphamide augmented induction of antitumor cells and antitumor resistance in C57BL/6 mice pretreated with mitomycin-C-treated EL4 cells (EL4MMC) plus OK-432, a streptococcal preparation. C57BL/6 mice were pretreated with EL4MMC (10(7] plus OK-432 (2.5 KE) i.p. twice at 1-week intervals. When the mice received an i.p. injection of cyclophosphamide at 200 mg/kg 2 days before the last treatment, the antitumor activity of their spleen cells and peritoneal exudate cells (PEC) was effectively augmented 7-8 days after the last treatment. Splenic antitumor activity disappeared 15 days after the last treatment whereas augmented antitumor activity of the PEC was detected even 28 days after the last treatment. This cyclophosphamide effect was dose-dependent and 200 mg/kg was the most effective among the doses tested. If the EL4MMC plus OK-432 treatment was injected at a s.c. site, it was also effective in combination with cyclophosphamide. The antitumor activity of the PEC from s.c.-pretreated mice, however, was lower than that from i.p.-pretreated mice. Despite the fact that cyclophosphamide effectively augmented induction of antitumor cells in C57BL/6 mice pretreated with EL4MMC plus OK-432, it diminished rather than augmented, under all conditions tested, the ability of the mice to resist a challenge of live EL4 cells. Reduction of antitumor resistance by cyclophosphamide was also observed in an experimental system of a semi-syngeneic host (BDF1) tumor (EL4). These results indicate that augmentation of in vivo induction of certain kinds of antitumor cells does not necessarily result in a beneficial augmentation of the host's ability to resist tumor growth.

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“…Several laboratories have tried to relate the systemic studies to the host response within the tumour, in an attempt to identify the important effector mechanisms responsible for regression. Cytotoxic T cells (Plata & Sordat, 1977;Holden et al, 1976;Gillespie et al, 1977;Chapdelaine et al, 1979), cytolytic macrophages and cytostatic macrophages (Puccetti & Holden, 1979;Russell et al, 1977) have been isolated from enzymedispersed tumours induced both by MSV and by the MSC tumour line established from an MSV-induced sarcoma. Studies carried out on both systemic and intratumoral immunity to MSV in A/Sn mice, however, indicated that cytotoxic T cells are not induced in this strain, suggesting that cytotoxic T cells might not be essential for the regression of MSV-induced tumours (Becker & Klein, 1976.…”

Section: Discussionmentioning

confidence: 99%

“…It has been classified as a true malignancy (Perk & Moloney, 1966) as well as a reparative granulomatous process (Stanton et al, 1968;Siegler, 1970). The regression of the lesion is T-cell-dependent Gorezynski, 1974;Stutman, 1.975) and cytotoxic T cells have been found in lymphoid organs and blood as well as within the tumour mass in C57BL and BALB/c mice (Plata & Sordat, 1977;Holden et al, 1976;Gillespie et al, 1977). Thus cytotoxic T cells are considered to play an important role in regression.…”

mentioning

confidence: 99%

“…As these cells need not be the correct targets for the demonstration of cytotoxic T cells in this strain, though suitable in other strains (Plata & Sordat, 1977;Holden et al, 1976;Gillespie et al, 1977), we made an effort to isolate the in vivo target cells for the virus to use as in vitro targets in the cytotoxicity tests of the inflammatory cells isolated from the tumours. In this paper, we describe some properties of the MSV "sarcoma"* cells which qualify them as target cells for the in vitro testing.…”

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confidence: 99%

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In vitro demonstration of in situ autologous tumour-cell cytotoxicity in MSV-induced tumours in A/SN mice

Becker¹,

Haskill²

1981

Br J Cancer

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Summary.-Moloney sarcoma-virus (MSV)-induced tumours in A/Sn mice have been dispersed with collagenase and DNase 8-15 days after virus inoculation, and both "sarcoma" and inflammatory cells separated by sedimentation velocity and adherence techniques. The isolated "sarcoma" cells had the morphological characteristics of atypical cells (i.e. cytoplasmic blebbing, vacuolization and prominent nucleoli) and were easily adapted to in vitro growth. As few as 2 x 103 of these cells inoculated i.m. produced new tumours within 8 days of injection in both syngeneic and allogeneic mice. Also, cell-free supernatant from "sarcoma"-cell cultures produced tumours, indicating that the successful transplantation of the "sarcoma" cells was probably due to production of infective virus. Cells cytotoxic in vitro against the ''sarcoma'' cells were present within both spleen and tumour of the tumour donors, but not in the spleens of normal mice. The cytotoxicity was specific against virusinfected cells, since in a mixture of virus-positive (gp 70) and virus-negative cells, positive cells were removed while negative cells were not affected, as measured by a visual cytotoxicity assay using immunostaining. Although T cells could be isolated from the MSV-induced tumours, these cells did not appear to mediate the cytotoxicity detected against the MSV "sarcoma" cells. These results suggest that early MSV infections might be sensitive to cytotoxic mechanisms distinct from those reported with established MLV-or MSV-induced tumour lines.

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Murine sarcoma virus (msv)‐induced tumors in mice. I. Distribution of msv‐immune cytolytic t lymphocytes in vivo

Cited by 30 publications

References 25 publications

Immune surveillance and natural resistance: an evaluation

Immune surveillance and natural resistance: an evaluation

Augmented induction of antitumor cells in vivo by cyclophosphamide fails to benefit antitumor resistance of the host

In vitro demonstration of in situ autologous tumour-cell cytotoxicity in MSV-induced tumours in A/SN mice

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