Cell‐mediated and humoral immunity studies of murine and hamster sarcoma virus‐induced producer and non‐producer tumors in syngeneic animals

McCoy, J. L.; Ting, R. C.; McCoy, N T; Reisher, Joel I.; Chan, S. P.; Law, Lloyd W.

doi:10.1002/ijc.2910130517

Cited by 9 publications

(2 citation statements)

References 13 publications

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“…This report was contradicted, however, by the results of Ting and Herberman (45) employing the radiolabeled antibody technique. Similarly, in the case of mouse cells transformed by the nonproducer murine sarcoma virus (MSV), nonvirion, virus-specific tumor surface antigens could not be demonstrated by immunofluorescence or by lymphocyte cytotoxicity tests in vitro -and evidence for isograft resistance based on such surface antigens was not firm (46). This, too, was countered by serologic immunoferritin studies which indicated the presence of such an antigen in small amounts (47).…”

Section: Discussionmentioning

confidence: 85%

The expression and localization of surface neoantigens in transformed and untransformed cultured cells infected with avian tumor viruses

Phillips¹,

Perdue²

1976

J Supramol Struct

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The presence and localization of neoantigens induced in cultured cells, infected or transformed with avian tumor viruses (ATV), were studied ultrastructurally on carbon platinum replicas of cell surfaces. The use of antibody, labeled with hemocyanin molecules, provided sensitive detection and analysis of cell surface antigen distribution. The subgroup-specific antigens of the viral envelope were found in considerable amount in the plasma membranes of ATV-infected chick embryo fibroblasts. The distribution of these antigens over the cell surface, evaluated on cells which were prefixed with glutaraldehyde, was found to be diffuse with a greater density on the cell processes in some cells. Reaction of antibody to viral envelope antigens with living ATV-infected cells resulted in a number of patterns of redistribution of membrane antigen-antibody complexes (AAC). Redistribution occurred in symmetrical or asymmetrical modes. The former consisted of randomly oriented aggregates (patches) of AAC over the cell surface. The latter included: (a) linear accumulation of AAC at cell margins; and (b) condensation of compexes into one or more centers of coalescence. These observations could be made on chick embryo cells infected (but not transformed) by avian leukosis virus, or on cells oncogenically transformed by avian sarcoma virus. The regions of coalescence were suggestive of the "capping" phenomenon seen in other systems, and their formation was temporally correlated with endocytosis of labeled AAC and the gradual loss of AAC from the surface. The effects of several biologically perturbing substances on the processes of redistribution were investigated in ALV-infected fibroblasts. Sodium azide, puromycin, actinomycin D, and colchicine had no effect on either form of asymmetrical redistribution. Cytochalasin B (CB) and iodoacetic acid (IAA) appeared to have some effect on the marginal redistribution, and to completely prevent the condensation into foci of coalescence (FC). When treated with these compounds, reacted with antibody at low temperature, washed free of unbound antibody, and warmed at 37 degrees C, cells rapidly cleared their surfaces of AAC. This was not accompanied by formation of FC or endocytosis. In some of these cells, a distribution was observed which suggested a possible centrifugal flow of antigenic sites-perhaps an alternate route for disposal of AAC. None of the drugs tested affected symmetrical redistribution. Repeated attempts at detection and topographical analysis of a tumor-specific antigen on the surface of Rous sarcoma virus-transformed chicken and rat cells have provided no evidence for antibody to such an antigen in the serum of immunized animals. Autochthonous, homologous, and heterologous immunizations of chickens and rats did not produce a detectable antibody response to a virus-specific tumor surface antigen. Preliminary results, however, suggest the expression of an individual-specific (unique) tumor antigen on the surface of Rous sarcoma cells.

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Section: Discussionmentioning

confidence: 85%

The expression and localization of surface neoantigens in transformed and untransformed cultured cells infected with avian tumor viruses

Phillips¹,

Perdue²

1976

J Supramol Struct

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“…There exist numerous methods of potential value for detecting antibodies to tumor antigens in xenogeneic antisera prepared against cellular antigens (Ting and Herberman, 1976;Herberman, 1977). The array of technologies employed previously includes cytotoxicity (Schultz et al, 1975;Fritz e et al, 1976, Rosenberg et al, 1977, complement fixation (Lewis et al, 1969;Wood and Barth, 1974;Sabin and Tarro, 1973;Hollinshead et al, 1976;Rogers et al, 1977), isotopic antiglobulin binding assays (Harder and MacKhann, 1968;Sparks et al, 1969), immunofluorescence (Henle and Henle, 1966;Moller, 1961;McCoy et al, 1974) and antibody-dependent cellular cytoxicity (Perlman et al, 1972;Jolley et al, 1976). The discovery by Kronvall et al, (1970) that Staphylococcus aureus protein A (SPA can bind the Fc portion of several mammalian species of IgG provided the basis for development of new immunoassays to detect IgG antibodies and cellular antigens.…”

mentioning

confidence: 99%

Protein‐A antibody‐binding (PAAB) technique for detection of tumor‐associated membrane antigen (TAMA) of lewis lung carcinoma

Veltri

McKolanis

Rockoff

et al. 1980

Intl Journal of Cancer

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Xenoantisera were prepared in rabbits against intact paraformaldehyde-fixed Lewis lung carcinoma (LLCa) cells and membrane solubilized proteins extracted with Triton X-100 and 3M KCI. The antisera were analyzed for antibodies to tumor-associated membrane antigens (TAMA) by means of a solid-phase radioimmunoassay (RIA). THe immunoassay employed 125-labelled Staphylococcus aureus protein A (SPA) to detect specific antibody binding to glutaraldehyde-fixed Lewis lung tumor target cells. The protein-A antibody-binding (PAAB) method is rapid, sensitive and reproducible. The PAAB revealed a possible LLCa-TAMA as evidenced by the reactivity of xenoantisera raised to LL paraformaldehyde tumor cell vaccine (TCV) and LL tumor Triton X-100 (TTri) and 3M KCI (TKCI) extracts of membrane preparations. The reactivity of our antisera followed linear dose-response kinetics but the degree of reactivity decreased from anti-TCV to anti-TTri to anti-TKCI respectively. The LL-TAMA demonstrated specificity since our antisera did not significantly cross-react with normal C56BL/6 cellular antigens or other known murine tumor-associated surface antigens of virally and chemically-induced tumor systems.

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Studies of lymphocyte stimulation by intact tumor‐cell and solubilized tumor antigen

Dean

McCoy

Lewis

et al. 1975

Intl Journal of Cancer

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BALB/c mice were rendered immune to syngeneic SV40-induced sarcoma by subcutaneous injection of mKSA-TU5 tissue-culture adapted cells. Spleen cells from immune mice were examined for tumor-cell neutralization in the Winn assay as well as in in vitro lymphocyte stimulation assays. A microculture (200 mul) lymphocyte stimulation (LS) assay utilizing immune spleen cells was employed with mixed lymphocyte/tumor-cell cultures (MLTC) and the papain crude soluble (CS) extracts from mKSA-TU5 cells. Specificity in the LS assay was determined using spleen cells from mice immune to other syngeneic tumors and by soluble antigenic preparation of normal BALB/c spleen cells. The Winn assay studies demonstrated that spleen cells from mKSA-sensitized mice neutralized mKSA tumor cells and this was corroborated by their resistance to direct tumor challenge. Positive lymphocyte transformation responses in MLTC were observed when mKSA-TU5-sensitized spleen cells were mixed with mitocycin-C-treated intact tumor cells or when papain-solubilized antigens of mKSA cells were employed, but not with non-immune spleen cells or with a soluble antigen from normal cells. Papain-solubilized antigen preparations employed in in vitro assays also immunized against challenge with mKSA tumor cells. Specificity of these lymphocyte transformation reactions was demonstrated with non-sensitized lymphoid cells or lymphoid cells from mice sensitized with a syngeneic Kirsten virus-induced respond. Thus, mKSA tumor surface antigens were recognized on intact tumor cells or with microgram quantities of papain-solubilized extracts from these tumor cells. We believe the lymphocyte stimulation assay affords a method for demonstrating the presence of tumor-specific antigen and for monitoring further purification procedures.

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Cell‐mediated and humoral immunity studies of murine and hamster sarcoma virus‐induced producer and non‐producer tumors in syngeneic animals

Cited by 9 publications

References 13 publications

The expression and localization of surface neoantigens in transformed and untransformed cultured cells infected with avian tumor viruses

The expression and localization of surface neoantigens in transformed and untransformed cultured cells infected with avian tumor viruses

Protein‐A antibody‐binding (PAAB) technique for detection of tumor‐associated membrane antigen (TAMA) of lewis lung carcinoma

Studies of lymphocyte stimulation by intact tumor‐cell and solubilized tumor antigen

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