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Query: UMLS:C0153470 (Spleen)
 4,015 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

[(3)H]Thymidine-labeled tumor cells are used to evaluate the cytotoxic cellular immune response against tumor-specific antigens; the loss of label due to destruction and detachment of target cells from the surface of the culture vessel is measured. Spleen cells from mice immunized against Moloney virus-induced rhabdomyosarcoma specifically destroyed the sarcoma cells, while cells from normal syngeneic mice did not. Peripheral blood lymphocytes from patients with malignant tumors were specifically cytotoxic to autologous tumor cells and to allogeneic tumor cells histopathologically identical to the autologous tumor, but not to autologous nonmalignant fibroblasts, or to allogeneic tumor cells from a histologically dissimilar tumor. Serum from the same patients specifically protected autologous tumor cells from lymphocyte cytotoxicity. This serum-mediated protection of tumor cells against autologous cellular immunocytotoxicity also extended to histologically identical allogeneic tumor cells. Cross-reactivity of anti-tumor cellular immunocytotoxicity in vitro, and its "blocking" by autologous serum, strongly suggest the presence of common tumor antigens. The antagonism demonstrated in vitro between serum and cellular immunity may explain the continued growth of malignant tumors in the face of demonstrable cellular immunity.
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PMID:In vitro detection of cytotoxic cellular immunity against tumor-specific antigens by a radioisotopic technique. 433 Oct 89

Spleens from Moloney sarcoma virus (MSV) tumor-bearing C57BL/6N mice contained four times the normal number of mononuclear cells and displayed a markedly elevated "spontaneous" (mitogen-independent) DNA synthesis on a per cell basis. The number of macrophages were increased three-fold while there was a slight reduction in the percentage of T lymphocytes. The phytohemagglutinin (PHA) response on a per cell basis of spleens from tumor-bearing mice was decreased about 90% when compared with normal control mice. The primary in vitro immune response to sheep red blood cells was also suppressed to levels of less than 10% of normals. The PHA response could be restored by purification of MSV spleen cells by rayon adherence columns and by removal of phagocytic cells by an iron/magnet technique. The activity of suppressor cells in MSV spleens was demonstrated in mixtures with syngeneic normal spleen cells where a marked impairment of the PHA response was observed. Spleen cells from tumor-free nude mice and normal spleen cells treated by anti-theta serum plus guinea pig complement (C'), both totally unreactive to PHA, had no such effect. The inhibitor cell in MSV spleens was shown to be insensitive to inactivation by anti-theta plus C', but could be removed by the adherence columns and the iron/magnet technique. These data suggest that this suppressor cell is a cell of the monocyte/macrophage series. Suggestive evidence was also presented that the suppressor cells belong to a proliferating population in MSV spleens. Similar suppressor cells have been previously demonstrated in spleens of mice during a variety of immune responses. Our data show, that a tumor, although stimulating the immune system, nevertheless may be suppressive on certain immune functions through the activation of suppressor cells.
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PMID:Evidence of suppressor cell activity in spleens of mice bearing primary tumors induced by Moloney sarcoma virus. 459 16

The role of Ia-positive accessory cells in the generation of a secondary cytotoxic response to tumor-associated antigens induced by Moloney murine sarcoma virus (M-MSV) was evaluated. Spleen cells from M-MSV-immune A.TL mice, depleted of accessory cells by anti-Iak serum plus C treatment and stimulated in secondary mixed leukocyte tumor cell culture (MLTC) with syngeneic Ia-negative A6ATL Moloney leukemic cells, failed to generate virus-specific cytotoxic T lymphocytes (CTL). CTL generation in Ia-depleted MLTC may be reconstituted by the addition of nonimmune Ia-positive spleen or peritoneal cells obtained not only from syngeneic A.TL but also from I-incompatible A.TH mice. This lack of restriction observed in accessory cell function is explained in terms of a nonspecific mechanism of CTL triggering mediated by soluble factors. In fact, IL 2 as well as supernatants obtained from I region-incompatible cultures consisting of M-MSV-immune, Ia-depleted A.TL spleen cells and A.TH Ia-positive cells, reconstituted secondary virus-specific CTL generation.
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PMID:Role of accessory cells in the induction of a secondary cytotoxic response to Moloney murine sarcoma virus-induced tumors. 618 89

The use of monoclonal antibodies to distinguish human sarcoma from carcinoma cells has been explored. Spleen cells from a BALB/c mouse immunized with a human malignant fibrohistiocytoma were fused with cells of the mouse P3U1 plasmacytoma cell line. Antibodies were then screened for reactivity against human sarcoma and carcinoma cells growing in culture. This work has yielded 2 immunoglobulin G monoclonal antibodies VIE4 and VIF3 which, respectively, reacted with 85% (17 of 20) and 90% (18 of 20) of sarcoma lines tested but with none of eight carcinoma cell line preparations. Reactivity against normal fibroblasts was also demonstrated. By immunofluorescence, the antigens detected by the two antibodies appear to have distinctive intracellular distributions. Immunoprecipitation with VIF3 has shown that it is detecting a protein with a molecular weight of 70,000. When tested against pathological frozen tissue sections, VIF3 reacted with four of 11 and VIE4 with three of 11 human sarcomas but with none of ten carcinomas tested. VIF3 occasionally bound to normal adult connective tissues, whereas no such reactivity was seen with VIE4. These antibodies appear to be directed to fibroblastic markers associated with sarcomas and connective tissue differentiation antigens.
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PMID:Monoclonal antibodies to human sarcoma and connective tissue differentiation antigens. 620 2

Spleen cells from BALB/c mice bearing a small, but already clinically evident transplantable methylcholanthrene-induced sarcoma (CE-2) are not able to release interferons, proliferate and perform a cytotoxic response against CE-2 cells, nor able to inhibit their growth in vivo in a Winn-type neutralization assay. They can, however, be reeducated to be efficiently active against the tumor. Spleen cells (25 X 10(6) ) and 10(6) mitomycin C-treated CE-2 cells were cultured in 20 ml of medium for 6 days. The surviving spleen cells were then cultured for another 5 days under the same conditions plus 10% interleukin 2-rich supernatant from a clone of EL-4 thymoma cells stimulated with phorbol-12-myristate-13-acetate. Reeducated spleen cells were then able to inhibit the growth of a 100% lethal dose of CE-2 tumor cells in a Winn-type assay, even when the lymphocyte to tumor cell ratio was 5:1. In vitro, they released interferon-gamma when restimulated by CE-2 cells, and displayed a marked cytotoxicity in an 18-hr assay. Their in vivo tumor-neutralizing activity was not affected by the removal of Lyt-2.2+ lymphocytes, nor by the absorption of cytolytic cells on CE-2 monolayers. The absorbed cell population no longer contained cytotoxic cells nor cytotoxic cell precursors, but still contained CE-2-specific helper cells, which assist the in vitro induction of cytotoxic cells by normal thymocytes. Lyt-2.2-, noncytotoxic, reeducated spleen cells from tumor-bearing mice thus play an important role in tumor neutralization in vivo.
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PMID:In vitro reeducated T helper cells from sarcoma-bearing mice inhibit sarcoma growth in vivo. 622 83

To specify the mechanism whereby inoculation of sarcoma viruses protects against leukemia development by leukoviruses, several experiments were performed using Friend virus complex (FVC) and MSV-F, a sarcoma virus pseudotype prepared in vitro with FVC as source of the helper component. The sarcomatous lesions induced by MSV-F were self-limited, irrespective of dose and route of inoculation and protected against the progressive, lethal erythroleukemia induced fy FVC. The sera of MSV-F primed mice had high FVC-neutralizing titers, Out of 3 properties titered in FVC, immunogenicity, XC-syncytium-forming activity and lethality, the frmer two were retained at high titers in MSV-F, while lethality was almost entirely lost: the dose-range between lethal immunizing dilutions was 2-3 logs broader for MSV-F than for FVC. It is postulated that the lethal, early erythroleukemia inducing component (Spleen Focus Forrming Virus) is rapidly lost from FVC upon in vitro propagation. The rescued MSV-F would carry a hightitered, immunogenic and Xc-syncytium forming component (Lymphatic Leukemia Virus), thus behaving as an immunogenic virus of limited pathogenicity.
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PMID:Immunity to Friend virus complex: analysis of protection with a sarcoma virus pseudotype. 625 97

We have evaluated the stimulation of target cell growth in vitro by spleen cells from mice which were immunized with polyoma-transformed cells and other tumor and non-tumor antigens. Stimulation was particularly seen under conditions of immunization that were suboptimal for the production of specific cytotoxicity. Significant stimulation of polyoma target cell growth was observed by lymphocytes from mice immunized against 10(5) Py 4198 tumor cells. This stimulation of target cell growth was not confined to polyoma-transformed cells only. Cells transformed by SV40, H-MuSV and non-transformed cells like 3T3 and embryo fibroblasts were also stimulated. Immunization of mice with syngeneic embryo fibroblasts also resulted in stimulation of tumor cell growth by the spleen cells from the immunized mice. However, the growth stimulation was less consistent and did not occur in all target cells tested. The specificity of immunostimulation was further studied with the Moloney sarcoma virus (M-MuSV) system; an antigenically distinct tumor system. Spleen cells from M-MuSV tumor-bearing mice stimulated cell growth in vitro not only against MuSV-transformed cells but also with SV40-transformed and polyoma-transformed cells as targets. Significant stimulation of target cell growth was also observed by spleen cells from mice that were immunized against 'non-pertinent' antigens, e.g. sheep red blood cells and allogeneic (C57B 1/6) spleen cells.
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PMID:Immune response to polyoma tumor cells in mice--III. Stimulation of tumor cell growth in vitro by spleen cells from immunized animals. 629 72

Murine sarcoma virus (MSV)-immune T cells from C57BL/6 mice respond to intact RBL-5 tumor cells with the production of leukocyte adherence inhibition factor (LAIF), which mediates an adherence inhibition response of macrophages. LAIF is elaborated by isolated Lyt-2+ cells incubated with RBL-5 cells, whereas Lyt-1+ cells elaborate a substance that enhances macrophage adherence. Spleen macrophages or peritoneal exudate macrophages from MSV-immune mice when present at concentrations of 0.1% changed the response of Lyt-1+ cells from the formation of an adherence enhancing factor to the formation of an adherence inhibiting factor. Migration inhibition factor (MIF) was formed by Lyt-1+ cells, but not by Lyt-2+ cells under identical culture conditions. Addition of either spleen macrophages from mice with progressively growing tumors or tumor-infiltrating macrophages suppressed LAIF formation by both Lyt-1+ and Lyt-2+ cells. Tumor-infiltrating macrophages elicited an adherence enhancing factor from Lyt-2+ cells when present at high concentrations. The results suggest that the extent of macrophage adherence in vitro is the outcome of an interaction of macrophages with mediators that have opposing effects.
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PMID:Leukocyte adherence inhibition response to murine sarcoma virus-induced tumors. II. Requirement for T-cell subpopulations and macrophages. 630 31

Spleen cells from mice bearing large methylcholanthrene (MCA)-induced sarcomas were injected intravenously into mice challenged in the hind footpads with heavily-irradiated cells from the same or a different sarcoma. As measured by [3H]-thymidine incorporation on day 5 or 6, cellular proliferation in the draining popliteal lymph nodes of these mice was significantly depressed as compared to control animals receiving normal spleen cells or medium intravenously. The suppression was found to be mediated by a Qa-1-positive, Thy-1 positive cell. It was relatively resistant to cyclophosphamide treatment (100 mg/kg). Furthermore, it had both antigen-specific and non-specific components. The findings are discussed in relation to a suppressor activator cell-suppressor acceptor cell pathway in the immunoregulation of tumor immunity.
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PMID:Suppressor pathways in tumor immunity: a requirement for Qa-1 positive tumor-bearer spleen T cells in suppression of the afferent immune response to tumor antigens. 645 94

Tumor-cell proteins that were antigenic in a syngeneic animal were identified by immunoprecipitation with monoclonal antibodies. Spleen cells of BALB/c mice immunized with plasma membranes of Kirsten RNA sarcoma virus-transformed BALB/3T3 cells were fused with NS-1 myeloma cells. Antibodies secreted into the culture fluid from these hybridomas were distinguished by their reactivity against proteins of different target cells. A total of 191 cultures were established; 143 produced antibodies that bound to BALB/3T3 cells transformed by the RNA sarcoma virus, of which antibodies from 82 bound to BALB/3T3 transformed with simian virus 40, and antibodies from 56 bound to BALB/3T3 cells. Thus, more than 50% of the cultures produced antibodies that possibly were specific to antigens of the transformed cell. Twenty different hybridomas have been cloned, and antibodies, from eight of these were found to immunoprecipitate five different proteins. A protein of approximately 32,000 daltons was precipitated from BALB/3T3 cells transformed by the RNA sarcoma virus, simian virus 40, or methylcholanthrene but not from untransformed BALB/3T3 cells. A protein of about 300,000 daltons was precipitated from all four cell lines; precipitation was enhanced in the viral transformed cells. Proteins of approximately 57,000, 54,000, and 8500 daltons were immunoprecipitated from all four cell lines.
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PMID:Transformation-related antigens identified by monoclonal antibodies. 693 18


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