Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0153470 (Spleen)
4,015 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Plasmacytomas are induced in BALB/c mice by the intraperitoneal injection of pristane (2,6,10,14-tetra-methylpentadecane) after a latent period of six months and more [Anderson, P. N. & Potter, M. (1969) Nature 222, 994-995]. Spleen cells mesenteric lymph node cells, thoracic lymph node cells, and peritoneal exudate cells were prepared from pristane-treated and control uninjected BALB/c mice during the course of a 10-month period, and these cell suspensions were tested for the release of infectious murine leukemia viruses. Endogenous ecotropic and xenotropic murine leukemia viruses were expressed in pristane-treated mice during the latter part of the tumor induction period, in those cell populations in which transformed plasma cells appear, namely, peritoneal exudate cells and thoracic lymph node cells. The significance of preferential expression of both ecotropic and xenotropic murine leukemia virus in target cell populations following the administration of a carcinogen is discussed in terms of the possible formation of an oncogenic variant virus.
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PMID:Endogenous RNA tumor viruses are activated during chemical induction of murine plasmacytomas. 21 59

The human lympholine osteoclast activating factor (OAF) is thought to be involved in several bone-destroying diseases. The current studies were designed to produce monoclonal antibodies against OAF for use in the subsequent design of immunoassays for OAF in clinical samples. Spleen cells from mice immunized with purified human OAF were hybridized with mouse plasmacytoma cells in vitro to yield hybridomas. Several clones of these hybridomas secreted into the culture medium antibodies, which neutralized the biological activity of OAF at dilutions as high as 1:100,000 relative to the initial culture medium. These antibodies did not interfere with the activities of parathyroid hormone in the same systems. These results represent the first report of monoclonal antibodies against a human lympholine, and validate the concept that hybridoma production is a useful technique for developing antibodies against weak or scarce antigens.
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PMID:Production of hybridomas secreting monoclonal antibodies against the lympholine osteoclast activating factor. 22 47

Spleen cells from mice immunized with a cultured human neuroblastoma were hybridized with the mouse plasmacytoma P3X63Ag8. Hybrid myelomas were screened for production of antibodies that reacted with human neuroblastomas but not with cells from other tissues. One of these hybridoma antibodies reacted with an antigen present on the six human neuroblastomas tested, one of two retinoblastomas, a glioblastoma, and fetal brain, but did not react with other tumors or tissues including adult human brain.
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PMID:Hybrid myelomas producing antibodies against a human neuroblastoma antigen present on fetal brain. 42 40

BALB/c mice immunized with Nonidet P-40 (NP-40) crude solubilized (CS) extracts of a syngenetic methylcholanthrene-induced BALB/c sarcoma (Meth A) were challenged with viable Meth A cells to determine the ability of the solubilized preparations to induce transplantation rejection. Animals resisting such challenge were then used in agarose microdroplet macrophage migration inhibition (MMI) and tumor cell neutralization (Winn) assays to evaluate the antigenic specificity of these CS extracts. Spleen cells from those animals that rejected Meth A after immunization with the NP-40-solubilized preparations effectively neutralized the tumor-producing capacity of Meth A tumor cells as determined in Winn assays. MMI assays were quite sensitive and detected migration inhibition of peritoneal exudate (PE) cells from immunized mice with extract concentrations as low as picogram quantities. Specificity studies demonstrated that Meth A expressed no antigenic cross-reactivity with similarly prepared extracts of an unrelated SV40-induced sarcoma (mKSA), nor with a mineral oil-induced plasmacytoma (ADJ-PC5) of BALB/c mice. Inhibition of PE cell migration was mediated by culture supernatants (presumably migration inhibition factor [MIF]) generated from a mixture of immune spleen cells and mitomycin C (MMC)-treated Meth A cells as assayed in an indirect MMI test.
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PMID:Cellular immunity to solubilized tumor antigens of a methylcholanthrene-induced sarcoma with a migration inhibition assay. 65 88

E mu-myc transgenic mice were back-crossed to BALB/c mice up to back-cross generation 3. The offspring that included transgene-carrying and -negative mice in approximately equal proportions were randomly divided into 2 groups. Thirty-four mice (group I) were treated with pristane, followed by A-MuLV, and 40 (group II) were injected with A-MuLV alone. Altogether, 16 lymphoid tumors developed in group I and 17 in group II. Nine of the tumors in group I and 4 in group II appeared as ascitic tumors. The ascites contained lymphoblasts and 10 to 45% plasmacytoid cells. These tumors were designated as plasmablastic lymphomas (PLs). All tumors except one were transgene-positive and did not carry translocations. An exceptional tumor in group I carried a variant 6;15 translocation but not the transgene. It obviously corresponds to the regular Abelson + pristane-induced plasmacytoma. Among 11 tested PLs, 10 had a single retroviral insertion site, while one tumor showed 3. Among 18 untreated transgenic descendants (group III), chosen randomly during serial back-crosses, 15 (83%) developed lymphomas, with no sign of plasmacytoid differentiation. The incidence was comparable in all 3 groups, assuming 50% of the mice in groups I and II to be transgenic. The time distribution of tumor development was also similar. Spleen cells from transgene-carrying mice with no clinical sign of lymphoma were infected in vitro with A-MuLV and transplanted i.p. into BALB/c recipients. PLs developed in 26 of 31 pristane-treated recipients, but in only one of 18 untreated recipients. One of 6 PLs tested was monoclonal, whereas the remaining 5 were oligoclonal. They all expressed v-abl. These results show that some of the preneoplastic B-cells that expressed constitutively active myc transgene turned into plasmablasts after infection with A-MuLV. Full development of their neoplastic potential was facilitated by the presence of pristane-granuloma.
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PMID:Abelson murine leukemia virus transforms preneoplastic Emu-myc transgene-carrying cells of the B-lymphocyte lineage into plasmablastic tumors. 222 13

A spontaneously transformed T suppressor (Ts) clone, A12-D11/t, is described which arose from the antigen-specific Ts clone A12-D11 isolated from cells of the inguinal lymph node of a BALB/c mouse bearing the syngeneic plasmacytoma ADJ-PC-5. A12-D11/t Ts cells suppress in vitro specifically a primary syngeneic cytotoxic antitumor response with the consequence that no ADJ-PC-5-specific cytotoxic T cells can be generated. The in vivo effects of A12-D11/t Ts cells were studied by injecting them into BALB/c mice. Spleen cells from those mice subsequently failed to respond against ADJ-PC-5 plasmacytoma cells, whereas their response against other syngeneic BALB/c tumors remained unaffected. By using a model system which allows us to study the host's immune reactions to the antigenic load corresponding to initial stages of tumorigenesis, it has been shown previously that ADJ-PC-5-specific Ts cells are activated before the antigen threshold for the activation of cytotoxic T cells is reached. Regarding its phenotype and specificity, the A12-D11/t Ts clone seems to be the exact counterpart of such a Ts cell, and is therefore of special interest in the study of the role of Ts cells preventing immunity against a growing tumor.
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PMID:Isolation and characterization of in vitro and in vivo functions of a tumor-specific T suppressor cell clone from a BALB/c mouse bearing the syngeneic ADJ-PC-5 plasmacytoma. 241 9

Murine plasmacytoma MOPC 104E-K181 is a tissue culture cell line of MOPC 104E derived from BALB/c mice. MOPC 104E-K181 implanted subcutaneously in syngeneic normal mice regresses spontaneously after an initial growth of about 10 mm. Mice that regressed tumors or mice immunized intraperitoneally with mitomycin C-treated MOPC 104E-K181 myeloma could reject subsequent challenge of viable K181 myeloma cells. In contrast to euthymic mice, T-cell-deficient athymic nude mice developed subcutaneous tumors after challenge and died from progressive tumor growth, suggesting the critical role of T cells in tumor regression. In vitro induction of cytotoxic cells was used to define the immunologic mechanism by which the host can suppress tumor growth. Spleen cells from immune mice did not show cytolytic activity in 51Cr release cytotoxicity assay, but showed inhibitory action of tumor proliferation in vitro at an effector cell to target cell ratio of 500:1 in a [3H]thymidine incorporation assay. To determine if cytotoxicity could be induced against MOPC 104E-K181 cells, in vitro sensitizing cultures were studied. We have demonstrated that normal BALB/c spleen cells became cytotoxic against MOPC 104E-K181 cells after 5 days cultivation with mitomycin C-treated stimulator cells at an optimal responder to stimulator cell ratio of 5:1. Treatment of anti-Thy-1.2 serum plus complement abolished cytotoxic activity of effector cells. Cytotoxic cells lysed not only MOPC 104E-K181 cells used for stimulation but also H-2k osteosarcoma cells. It was concluded that Thy-1.2-positive cytotoxic cells with nonspecific anomalous reactivity could be induced in murine plasmacytoma-stimulating cultures.
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PMID:Immunoregulation of murine plasmacytoma. I. Generation of anomalous killer cells in vitro by cocultivation with MOPC 104E. 256 19

MRL/Mp-lpr/lpr (MRL/l) mice spontaneously produce antibodies to poly(ADP-ribose) that are cross-reactive with single stranded DNA (ssDNA). Spleen cells from these animals were used for fusion with murine plasmacytoma cells to prepare hybridomas that produce autoantibodies to poly(ADP-ribose). Monoclonal antibodies (MoAb) produced by the selected hybridomas not only preferred ssDNA to poly(ADP-ribose), but also reacted with left handed Z-DNA; the MoAb reflected the nature of serum antibodies to poly (ADP-ribose) in MRL/l mice. These results suggest that similar antigenic determinants exist in poly (ADP-ribose), ssDNA and left handed Z-DNA and that the cross-reactive nature of autoantibodies to poly (ADP-ribose) in MRL/l mice may be the results of expansion of such clones as selected in this experiment.
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PMID:MRL/Mp-lpr/lpr mouse derived monoclonal antibodies that recognise determinants shared by poly (ADP-ribose), single stranded DNA and left handed Z-DNA. 257 6

In order to clarify the effect of recombinant human tumor necrosis factor (rHu-TNF) on the antitumor T cell immune response, we examined the effect of rHu-TNF on the generation of cytotoxic T cells (CTL) against syngeneic tumor cells. Spleen cells from X5563 plasmacytoma-transplanted mice were stimulated in vitro with mitomycin C-treated X5563 cells in the presence or absence of rHu-TNF. The generation of CTL was augmented in a dose-dependent manner by the addition of rHu-TNF. The augmenting effect of rHu-TNF was more marked when indomethacin was added to the culture. The augmenting effect was observed only when rHu-TNF was added at the early stage of the generation of CTL. The cell surface phenotype of CTL generated was L3T4- and Lyt2+. The augmentation was shown not only by the chromium-51 release assay but also by the Winn assay. As to the specificity, the augmentation of CTL generation was observed by the addition of rHu-TNF when responder-primed spleen cells were stimulated with the tumor cells in vitro. On the other hand, augmentation was not observed when responder spleen cells were not stimulated with the tumor cells in vitro, or when responder spleen cells were obtained from normal mice. The CTL generated was not cytotoxic against other tumor cells of the same haplotype. Thus, rHu-TNF augmented the generation of CTL against syngeneic tumor cells in an antigen-specific manner. The in vivo effect of rHu-TNF was examined by administering rHu-TNF into X5563-bearing mice. The spleen cells of rHu-TNF-injected mice generated a much higher CTL activity against X5563 cells in vitro than did the spleen cells of uninjected mice. From these results, a possibility can be considered that in some cases, rHu-TNF may exert its antitumor activity by stimulating the immune system.
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PMID:Augmentation of the generation of cytotoxic T lymphocytes against syngeneic tumor cells by recombinant human tumor necrosis factor. 264 56

The occurrence of tumor immunity in mice bearing a growing plasmacytoma (PC) was studied by local adoptive transfer assay. Spleen cells from mice with a large PC but not with a nonpalpable or small PC retarded and often inhibited entirely the growth of homologous PC. They occasionally caused late regression of growing homologous and heterologous PC. The individual tumor-specific immune effector cells were found to be radiosensitive, non-adherent, Thy 1-positive T-cells. They were resistant to treatment of mice with high-dose cyclophosphamide (CTX). Their generation, however, was abrogated by low-dose CTX and irradiation at the early stage of their development. Spleen cells from PC-bearing mice treated with high-dose CTX were enhanced in their effector activity, suggesting the co-existence of CTX-sensitive suppressor cells. The suppressor cells could be demonstrated in spleens of mice bearing a heterologous PC and were found also to be radiosensitive, non-adherent, Thy 1-positive T-cells. Their generation was blocked by treatment of mice with CTX during the early stage of PC development. These findings provide evidence for the occurrence of immune effector T-cells in mice with a growing PC. This immunity appears to be down-regulated by CTX-sensitive suppressor cells.
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PMID:Splenic immune effector and suppressor cells in mice bearing a growing plasmacytoma. 293 18


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