UMLS:C0153470 - FACTA Search

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

BCG (Bacillus Calmette-Guerin) vaccine, Tice strain, caused a threefold increase in spleen weight of normal animals and a fourfold increase in spleen weight of sarcoma-bearing mice. In the latter group, the BCG vaccine caused infiltration of the sarcoma cells into the peritoneum and tumor metastasis in the spleen. Spleen lymphocytes from mice immunized with neuraminidase-treated sarcoma or from mice that had overcome an inoculum (100 cells) and a challenge (10(4) cells) of sarcoma P-1798 were cytotoxic against 51 Cr- or 14C-2-thymidine-labeled sarcoma cells. The serum of these mice enhanced the cytotoxic activity and inhibited the migration of the syngeneic lymphocytes. These serums also inhibited the migration of peritoneal macrophages from guinea pigs immunized with the sarcoma cells. BCG vaccine enhanced the development and growth of sarcoma P-1798; i.e., 50-100 viable sarcoma cells produced solid tumors in 8% of the untreated animals but in 100% of the BCG-treated animals. The serum of BCG-treated sarcoma-bearing animals inhibited the spleen lymphocyte-mediated cytotoxic action. The spleen lymphocytes from the BCG-treated sarcoma-bearing animals had no effect against 51Cr- or 14C-2-thymidine-labelled sarcoma cells. The data indicate that the serum from BCG-treated sarcoma-bearing animals blocks the spleen lymphocyte-mediated cytotoxic activities directed against proliferation and growth of the sarcoma.
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PMID:Mechanism of action of BCG vaccine on neoplastic proliferation and host immune responses. 126 78

By using two different syngeneic tumors, Meth A sarcoma and RL male 1 lymphoma of BALB/c origin, the present study was designed to investigate the subset(s) of T cells mediating in vivo antitumor immune responses and some of the effector mechanisms of in vivo protective immunity in BALB/c mice immunized against tumor or bearing tumor. Spleen cells from the mice immunized against Meth A tumor or bearing Meth A tumor inhibited the growth of Meth A tumor in the Winn assay. In the Meth A-immunized mice, L3T4+ (CD4+) cells played a major role in mediating the inhibitory activity against Meth A tumor growth, whereas in the Meth A-bearing mice, the antitumor protective immunity was mediated by both L3T4+ and Lyt-2+ (CD8+) cells. Spleen cells from the Meth A-immunized or Meth A-bearing mice were not able to generate cytotoxic T lymphocytes (CTL) directed against Meth A tumor after the in vitro restimulation of spleen cells with mitomycin C (MMC)-treated Meth A cells, while fresh spleen cells from the Meth A-immunized or Meth A-bearing mice were able to induce the strong delayed-type hypersensitivity (DTH) responses to Meth A tumor. The DTH response to Meth A tumor was mediated by L3T4+ cells in the Meth A-immunized mice and by both L3T4+ and Lyt-2+ cells in the Meth A-bearing mice. In the similar experiments performed in the RL male 1 lymphoma, the antitumor activity in spleen cells from the RL male 1-immunized or RL male 1-bearing mice depended on Lyt-2+ but not L3T4+ cells in the Winn assay. When spleen cells from the RL male 1-immunized or RL male 1-bearing mice were cultured with MMC-treated RL male 1 cells for 5 days, an appreciable CTL response to RL male 1 tumor was induced. These results suggest that the nature of tumor and/or tumor antigens determines which T cell subset is required to exhibit the protective immunity against tumor and thus the different effector mechanisms could be induced in the different tumor models. Furthermore, these data support the conclusion that antitumor T cell responses are affected by the immune state of host to tumor.
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PMID:Effector phenotypes and mechanisms of antitumor immune reactivity of tumor-immunized and tumor-bearing mice in two syngeneic tumors. 167 79

Recombinant human interleukin-1 beta (IL-1 beta) inhibited the growth of not only the right, but also the left non-treated tumor in a double grafted tumor system. Since the antitumor activity of IL-1 beta against the right and left tumors was not seen in nude mice, lymphocytes have a key role in the antitumor effect of intratumoral administration of IL-1 beta. TIL (tumor-infiltrating leukocytes) obtained from left and right side tumors treated with IL-1 beta were examined by Winn assay for their antitumor activity against Meth-A sarcoma in BALB/c mice. TIL from the right side clearly inhibited the growth of admixed Meth-A cells, but control TIL did not. Spleen cells and right and left regional lymph node cells prepared from IL-1-treated mice were examined for Lyt-1, Lyt-2 and L3T4 phenotypes. The number of Lyt-1-positive lymphocytes increased in the spleen and in the right regional lymph nodes after intratumoral administration of IL-1. Isolated tumor cells obtained from the right tumor treated with IL-1 beta and the left side tumor on day 6 were cultured in RPMI 1640 with 10% fetal calf serum for 24 h. The culture supernatants were harvested and tested for the presence of chemotactic activity for neutrophils or macrophages. Significant neutrophil chemotactic factor and macrophage chemotactic factor activities were detected in the culture media from IL-1-treated tumor tissues cultured for 24 h. Neither significant neutrophil nor macrophage chemotactic activity was detected in the media from untreated tumor tissues. These results suggest that intratumoral administration of IL-1 first induces neutrophils and macrophages in the right tumor, then Lyt-1-positive cells in the right regional lymph nodes and in the spleen, and subsequently induces macrophages in the left, non-treated tumor.
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PMID:Antitumor effector mechanism of interleukin-1 beta at a distant site in the double grafted tumor system. 175 85

Mistletoe extracts have approval for clinical application. This warrants the quest for the definition of the active substances to optimize their application. Thus, the extent of immunomodulating and antimetastatic activity of the beta-galactoside-specific lectin from mistletoe extract (ML I) was investigated. In BALB/c-mice regular subcutaneous (s.c.) injections of small nontoxic doses of ML I yielded significant enhancement of peritoneal macrophage activity, as measured in chemiluminescence assays, as well as significant weight gain of thymus. Spleen weight, however, increased without statistical significance. To evaluate the anti-metastatic activity of ML I we intravenously (i.v.) inoculated sarcoma L-1 and fibrosarcoma RAW 117-H 10 cells which cause tumor colonization of lungs and livers in BALB/c-mice, respectively. After regular s.c. administration of ML I, the number of lung and liver tumor colonies significantly decreased in both experimental tumor models as compared to control mice which received injections of saline solution. Accordingly, ML I can be regarded as a potent immunomodulating and antimetastatic substance, which seems to be promising for clinical trials in human oncology.
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PMID:Influence of treatment with the immunomodulatory effective dose of the beta-galactoside-specific lectin from mistletoe on tumor colonization in BALB/c-mice for two experimental model systems. 193 21

A limiting dilution microculture system, supplemented with a source of interleukin-2 (IL-2), was employed to evaluate the frequency of Moloney-murine leukaemia/sarcoma virus (M-MuLV/M-MSV)-specific cytotoxic T-lymphocyte precursors (CTL-p) which also exhibited NK-like activity. Spleen cells, obtained from M-MuLV/M-MSV regressor mice, were restimulated in bulk secondary mixed leucocyte-tumour cell cultures (MLTC), and subsequently plated in a culture medium supplemented with two different supernatants (SN) produced following PMA-stimulation of the same EL-4 thymoma cell line. SN 20, obtained from the cell line maintained in vitro, contained IL-2 and only negligible amounts (less than 3 U/ml) of interferon (IFN), while SN 19, obtained after passage of the ascitic form of EL-4 thymoma in syngeneic mice, contained both IL-2 and IFN in high titres. The frequency of CTL-p specific for MBL-2 lymphoma cells was high and comparable in cultures supplemented with both SN (1/2 X 84 cells and 1/2 X 40 cells, respectively), while the frequency of CTL-p directed against NK-susceptible YAC-1 target cells was low in SN 20 (1/90 cells) and high in SN 19 (1/5 X 40 cells). An analysis of individual microcultures established at low cell dose (1 cell/well) indicated that specific and NK-like activity could be ascribed to the same precursor cells. Furthermore, using different long-term CTL clones, we observed that, after passage in SN 20, double-reactive clones gradually lose the capacity to lyse NK-susceptible targets, while most of MBL-2 specific clones acquired NK-like activity following a few passages in SN 19. Therefore, the induction of NK-like activity is reversible and may be modulated by soluble factors present in supernatant in which CTL clones are maintained. Double-reactive clones were unable to lyse NK-resistant allogeneic tumour cells or normal syngeneic blast cells. A few clones cross-reacting with H-2d alloantigens also exhibited NK-like activity when maintained in SN 19. The different pattern of CTL clone activity was associated with a morphological change in the clones themselves: the acquisition of double activity was accompanied by an increase in cell size and the appearance of numerous cytoplasmic granules. All CTL clones were phenotypically Thy-1+ and Lyt-2+ on indirect immunofluorescence and complement-dependent cytotoxicity investigation.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Reversibility of lymphokine-induced NK-like activity in virus-specific cytotoxic T-lymphocyte clones. 257 29

The hematopoietic disregulation in adult mice induced by the malignant histiocytosis sarcoma virus (MHSV) and the Harvey murine sarcoma virus (Ha-MuSV), which both possess c-Ha-ras-related oncogenic sequences, was investigated. Spleen focus formation induced by MHSV and Ha-MuSV was not restricted by the Fv-2 resistance locus in congenic DDD and C57BL/6 mice, unlike leukemogenesis induced by Friend virus, Rauscher virus, and the myeloproliferative sarcoma virus (MPSV). C57BL/6 mice were much more resistant to MHSV and Ha-MuSV-induced spleen focus formation than DDD mice regardless of their Fv-2 state. Infection of DDD mice with MHSV caused a systemic histiocytic neoplasia, best described as murine malignant histiocytosis. Transformed histiocytic cells proliferated excessively in the bone marrow, spleen, and lymph nodes and, in the final stages of the disease, in all major parenchymal organs. The Ha-MuSV caused a strikingly different benign histiocytic tumor in DDD mice and, unlike MHSV, did not induce a rapid, progressive splenomegaly in C57BL/6 mice. Infection of DDD mice with MHSV induced a rapid and synchronized depletion of early and late erythroid precursor cell pools. In MHSV-infected C57BL/6 mice comparable changes were observed with dissimilar kinetics. Macrophage colony-forming cells of MHSV-infected mice were increased in number and proliferated independently of stimulating growth factors. The disease induced by MHSV in mice can thus serve as a model for malignant histiocytosis in humans.
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PMID:Murine retrovirus-induced malignant histiocytosis, an experimental model for the disease in humans. 282 12

Monoclonal antibodies (MAbs) against sarcoma-associated cell membrane antigens were prepared by immunizing BALB/c mice with tumor cells from a human osteosarcoma, TPX, grown as a xenograft in athymic BALB/c nude mice. Spleen cells from immunized mice were hybridized with X-63 Ag. 8.653 mouse myeloma cells which yielded 260 growing hybridomas. Seven of these produced antibodies that bound to TPX cells and to cells from another osteosarcoma, but not to autologous skin fibroblasts. MAbs from 2 (TP-1 and TP-3) of these 7 clones did not cross-react with non-sarcomatous tumor cells or peripheral blood lymphocytes. Immunohistochemical studies on frozen tissue sections showed that the TP-1 (IgG-2a) and TP-3 (IgG-2b) antibodies had characteristic and identical specificity profiles. Binding of TP-1 (TP-3) was demonstrated to 15/15 (15/15) osteosarcomas, 3/3 (2/2) synovial sarcomas, 7/9 (6/8) malignant fibrous histiocytomas, 2/2 (1/1) malignant hemangiopericytomas, 1/2 (1/2) chondrosarcomas and 3/6 (1/3) unclassified sarcomas. The antibodies did not bind to any of 16 sarcomas belonging to other histological subtypes, including liposarcomas and leio- and rhabdomyosarcomas. Moreover, they failed to bind to sections of 66 different non-sarcomatous malignancies, or to any of a range of normal adult and fetal tissues, although some weak staining of proximal kidney tubules was seen. The restricted specificity of these antibodies to some major subtypes of human sarcomas makes them promising tools for identification and subclassification of sarcomas.
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PMID:New monoclonal antibodies specific for human sarcomas. 352 38

Spleen cells of BALB/c mice hyperimmunized with a transplantable methylcholanthrene-induced sarcoma Meth A (Meth A-Im-SPL) inhibited the growth of Meth A tumor in vivo in a tumor neutralizing test. Meth A-Im-SPL did not neutralize another antigenically distinct sarcoma, Meth 1, indicating that the antitumor activity is tumor specific. Lyt-1+2- cells of Meth A-Im-SPL (Im-Lyt-1+2-) were the effectors since in vitro treatment of Meth A-Im-SPL with anti-Thy 1.2 or anti-Lyt 1.2 antibody plus complement completely abrogated their neutralizing activity, whereas treatment with anti-Lyt 2.2 plus complement did not. To further confirm the effector activity of Im-Lyt-1+2- cells, T cell subpopulations were separated from Meth A-Im-SPL by the panning method. The purified Im-Lyt-1+2-, but not Im-Lyt-1+2+ cells neutralized the tumor in athymic nu/nu mice as efficiently as in +/+ mice, suggesting that the donor Im-Lyt-1+2- cells but not recipient T cells were primarily responsible for neutralizing the tumor. The present study, however, did not exclude the possible contribution of recipient T cells to the tumor neutralization and this is open to further investigation.
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PMID:The Lyt phenotype of the T cells responsible for in vivo tumor rejection in syngeneic mice. 353 58

Spleen cells and peritoneal exudate cells obtained from BALB/c mice which had received an i.p. injection of 0.1 mg of OK-432 4 days previous to sacrifice, were examined by Winn's neutralization assay for their antitumor activity against Meth-A sarcoma cells in BALB/c mice. Both of the cell preparations clearly inhibited the growth of admixed Meth-A cells, but when these same cell populations were treated on a Sephadex G-10 column, the effector activity seen in Winn's assay disappeared. The effector cells responsible for tumor inhibition were therefore considered to be cytotoxic macrophages. However, the inhibitory effect of these cytotoxic macrophages in Winn's assay was not evident in either X ray (300 rad)-irradiated BALB/c mice or in nu/nu BALB/c mice. These results indicate that the antitumor activity of cytotoxic macrophages is associated with a sequential immune mechanism in which T cells may play an important role.
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PMID:[Antitumor effect of OK-432 (3)--mechanisms of tumor growth inhibition by OK-432 induced activated macrophages]. 388 61

Thymus, spleen, and lymph node cells from different periods of Sarcoma I allograft development in untreated (Sa I) or xenogeneic antithymocyte serum-treated (ATS-Sa I) B10 mice were adoptively transferred to secondary B10 recipients. While in sublethally (4.3 Gy) irradiated recipient mice the tumor destructing activity was predominantly expressed, in untreated recipients of transferred cells it was mostly the tumor enhancing activity. Therefore, in further studies directed at the detection of tumor enhancing activity, the adoptive transfers were only performed in untreated recipients. Thymus cells both of Sa I and ATS-Sa I mice showed a tumor enhancing activity all through the followed period, with a peak between days 7 and 21, then it decreased. Also the spleen cells of both groups had a tumor enhancing effect all the time, with a peak of activity on day 7. Spleen and thymus cells of progressors enhanced the tumor growth slightly more strongly than did those of the regressors. The tumor enhancing activity of spleen cells was in the beginning period confined mainly to the polystyrene nonadherent fraction of cells, at later times, in the progressors it was manifested in the adherent as well as in the nonadherent fractions. In the population of lymph node cells, at the start of tumor regression (in Sa I mice on day 7, in ATS-Sa I mice on day 14), a tumor destructing activity was observed. In both groups this activity was at later times followed by a tumor enhancing activity. The interpretation of the tumor enhancing activity of thymus and spleen cells of Sa I and ATS-Sa I mice is complicated by the tumor enhancing activity of cells of normal mice without tumor (N).
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PMID:Immune response of mice to sarcoma I allograft studied by adoptive transfers of spleen, thymus, and lymph node cells to secondary recipients. 404 56

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