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)

A single intramuscular injection of MnC12 in mice caused an increase in macrophage functional activity. Spleen cell antibody-dependent cell-mediated cytotoxicity against both chicken erythrocytes and P815 tumor cell targets was enhanced 24 h following a single injection of MnC12. Enhanced antibody-dependent cell-mediated cytotoxicity activity following MnC12 treatment was not associated with a change in spleen cellularities compared with saline-injected mice. Resident peritoneal macrophages from mice injected intramuscularly with MnC12 displayed enhanced phagocytic activity for chicken erythrocytes in the presence or absence of opsonizing antibody. Enhanced cytolytic activity against P815 mastocytoma target cells and enhanced cytostatic activity against MBL-2 lymphoma target cells was also observed for nonelicited resident peritoneal macrophages from mice injected intramuscularly with MnC12. There were no differences in the cellularity or relative number of adherent cells obtained from the peritoneal cavity of saline or MnC12-injected mice. These enhanced macrophage functions were associated with the induction of increased interferon levels in mice injected with MnC12.
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PMID:Manganese chloride enhances natural cell-mediated immune effector cell function: effects on macrophages. 258 Aug 13

A new B-lymphoma cell line (DEAU-cell line) was established from a diffuse large-cell lymphoma (centroblastic type) and was successfully grafted in athymic nude mice. Monoclonal antibodies (MoAbs) were generated using splenocytes of DEAU-tumor bearing mice. Before the fusion experiments, cellular immunity of the mice bearing growing DEAU tumors was restored by injection of spleen cells from conventional Balb/C mice. Spleen cells from conventional Balb/C mice immunized with DEAU-cell line were also used for the generation of MoAbs. Four MoAbs (DBB.42 and DBA.44 from normal Balb/C mice, and DNA.7 and DND.53 from athymic nude mice) were investigated because they identified B-cell-associated antigens not destroyed by fixatives. DBB.42 recognized a pan-B cell-associated antigen (molecular weight (mol wt) = 45 Kd). DBA.44 detected a B-cell antigen (mol wt not determined) expressed on a subpopulation of B lymphocytes in the mantle zone of lymphoid follicles. DNA.7 also defined a B-cell antigen (43 Kd) mainly expressed on germinal center cells. Similarly, DND.53 recognized a B-cell antigen (two bands of mol wt 20 Kd and 35 Kd, respectively) mainly expressed on germinal center cells and mantle zone lymphocytes and interdigitating reticulum cells in the paracortical area. Major differences were found in the reactivities of these MoAbs on malignant lymphomas. DBB.42 was positive with almost all B-cell lymphomas and some T-cell lymphomas. Within the group of low-grade B-cell lymphomas, DBA.44 reacted principally with hairy-cell leukemia. DNA.7 reacted mainly with high-grade B-cell lymphomas with a weak positivity in low-grade B-cell lymphomas. DND.53 reacted with all but one B-cell lymphoma, cells of histiocytosis X, and Reed-Sternberg cells. These findings indicate that new MoAbs can be generated by using spleen cells from athymic mice bearing human tumors as well as by new lymphoid cell lines. The MoAbs so generated, as in the present study, are deemed potentially useful for the recognition of B-cell lymphomas in routine diagnostic histopathology. In addition, DND.53 could be of value for the diagnosis of histiocytosis X and the detection of Reed-Sternberg cells in Hodgkin's disease.
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PMID:Production of anti-B monoclonal antibodies (DBB.42, DBA.44, DNA.7, and DND.53) reactive on paraffin-embedded tissues with a new B-lymphoma cell line grafted into athymic nude mice. 267 17

Spleen cells from mouse bone marrow chimaeras were cultured in vitro in mixed lymphocyte cultures (MLC) or in the presence of interleukin 2 (IL-2) without the added alloantigen. Precursors for the nonspecific cytotoxic cells (in this study: lymphokine-activated killer (LAK) cells) lysing natural killer (NK) cell-sensitive YAC-1 lymphoma could be found 10-12 days after the bone marrow reconstitution, simultaneously with the appearance of the NK activity. The ability of LAK cells to lyse NK-resistant tumour targets as well was demonstrated using the P 815 mastocytoma cell line; reactivity against this target was demonstrable 1 week later than the appearance on YAC-1 lysing cells. Phenotypically LAK cells derived from spleen cell cultures of bone marrow chimaeras did not differ from LAK cells derived from normal spleen cell cultures: precursors resided within the Thy 1-, asialo-GM1+ cell population, and effectors expressed both of these antigens. Splenic NK cells of early bone marrow chimaeras (up to 14-18 days after the bone marrow reconstitution) were Thy 1+ cells, and thus LAK cells of bone marrow chimaeras were not derived from these Thy 1+ NK cells. The treatment of effector cells with anti-Thy 1 antibody plus complement (C) abolished the lytic activity totally. However, these cells were not cytotoxic T cells, since alloreactivity, as an indication of the T-cell cytotoxicity, could not be demonstrated until 4-5 weeks after the bone marrow reconstitution.
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PMID:Lymphokine-activated killer cells in mouse bone marrow chimaeras. The relationship to natural killer cells and to alloreactive cytotoxic T cells. 286 99

We have previously shown that YC8, a Moloney virus-induced BALB/c lymphoma, is susceptible to lysis by BALB/c anti-DBA/2 effector cells. To further evaluate the relationship between non-H-2 antigens of DBA/2 background and tumor-associated determinants, we investigated the pattern of cytotoxic and proliferative responses induced in BALB/c mice by immunization with YC8 lymphoma. Spleen cells from tumor-immunized animals were restimulated in vitro with YC8 cells and tested for cytotoxicity on target cells of different strains and haplotypes. Cytotoxicity was observed only against YC8, DBA/2 blasts, and P815 (a DBA/2 mastocytoma). BALB/c anti-YC8 effectors were equally blocked by unlabeled YC8 and P815 cells when assayed on YC8 labeled targets. A clonal analysis, however, revealed the existence of at least two types of effectors, one lytic for both P815 and YC8 cells, the other lytic for YC8 cells only. BALB/c anti-YC8 cells proliferate when stimulated both with YC8 and DBA/2 cells in the presence of accessory cells. When tested in an adoptive transfer assay, anti-YC8 cells given i.v. cured 100% of i.v. and 75% of i.p. tumor-injected mice, respectively. When given i.p. anti-YC8 effectors cured 100% of i.p. tumor-injected animals. These results confirm the expression of non-H-2, DBA/2-like antigens on the BALB/c lymphoma YC8 and reveal the presence of additional tumor-associated determinants; both sets of antigens may induce a cellular immune response and elicit immune lymphocytes which can eradicate YC8 cells in an adoptive immunotherapy assay.
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PMID:Analysis of the cellular immune response to and adoptive immunotherapy of a BALB/c lymphoma that cross-reacts with normal DBA/2 cells. 293 37

We report the immunological studies on three transplantable lymphoma lines that developed when CAF1 mice were injected with busulfan and chloramphenicol. The lymphoma cells displayed Thy-1.2, brain associated antigen, and H-2d alloantigen. They were negative for surface IgM and Ia antigens. Expression of T cell differentiation antigens differed among the three lines. The 508 tumour line displayed only Thy-1.2: 408 tumour line displayed Thy-1.2, Lyt-2.2 and TL; and 808 tumour line was positive for Thy-1.2, Lyt-1.2, Lyt-2.2 and TL antigens. We established in vitro culture lines from 508 and 808 lymphoma cells. The lymphoma cells did not respond to mitogens and antigens. The splenic cells from mice bearing 508 or 808 had decreased phytohaemagglutinin (PHA), concanavalin A (Con A) and mixed leucocyte responses (MLR). When mitomycin-C treated lymphoma cells from the tumour bearing mice were cocultured with normal splenic mononuclear cells, the 808 lymphoma cells suppressed the mitogenic responses of the normal cells more profoundly than 508 lymphoma cells. Adherent cells from both tumours suppressed the Con A responses of normal spleen cells. Cells from in vitro 508 or 808 cell lines had no effect on mitogenic responses of normal cells. Plasma from tumour bearing mice, but not the supernatants taken from cultures of these lymphoma cells, suppressed the mitogenic responses of normal lymphocytes. Spleen cells from normal CAF1 mice responded in mixed leucocyte tumour reactions (MLTR) when cocultured with lymphoma cells. Mice immunized with mitomycin-C treated tumour cells had greater response. Responder cells taken from mice with established 508 or 808 tumors had suppressed MLTR responses. Although prior immunization with tumor antigen increased the MLTR response, injection of live tumour cells into immunized mice resulted in a more rapid tumour growth and suppression of MLTR response.
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PMID:Busulfan and chloramphenicol induced T cell lymphoma: cell surface characteristics and functional properties. 294 60

In vivo, subclones derived from EL4 lymphoma cells generate suppressor T lymphocytes specific for anti-EL4 immune responses. Spleen cells of EL4-sensitized C57BL/6 mice down-regulate the in vitro induction of EL4-specific cytolytic T lymphocytes (CTL). In addition, EL4-sensitized spleen cells interfere with the antigen response of two T lymphocyte clones. These recognize, in an H-2b context, a self-antigen on spleen cells that is also expressed by transformed cells, including EL4. The simultaneous anti-self and anti-EL4 specificity of the helper and suppressor activities suggests, therefore, that they are the product of an in vivo autoimmune reaction to EL4. The anti-self suppression might aim to re-establish self-tolerance, at the same time down-regulating responses against immunogenic epitopes that are co-expressed with the self-antigen on the EL4 cells. This agrees well with our observation that suppressor T cells, apparently elicited by suppressogenic epitopes on non-immunogenic EL4 subclones, down-regulate the CTL response elicited by immunogenic EL4 subclones. The additional self-specificity of this suppression indicates that the suppressogenic epitopes at least in part represent EL4 self-antigens.
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PMID:Specific suppression elicited by EL4 lymphoma cells in syngeneic mice. Specificity includes self-antigens on EL4. 295 13

Spleen cells obtained from Lewis rats were cultured with 4 micrograms/ml Con A for 96 hr, and activated cells were fused with BW5147 mouse T lymphoma cells. Seven clones obtained by fusion expressed rat IL 2R. The expression of rat IL 2R on those hybrid cells could be up-regulated by IL 2 itself, ATL-derived factor, and TPA and CA++ ionophore. Those IL 2R could be down-regulated by murine MoAb ART-18 that detects rat IL 2R. All hybrid clones produced IL 2 constitutively. IL 2 produced by hybrid cells bound to its receptor and promoted the proliferation of hybrid cells in some clones. Incubation of cells with exogenous IL 2 resulted in the proliferation of hybrid cells, whereas the proliferation of some clones was inhibited by exogenous IL 2, indicating that IL 2 had bifunctional properties on cell growth. Rat IL 2R from 6H2-F9 hybrid cells was studied by both one- and two-dimensional SDS-PAGE with ART-18. The IL 2R derived from 6H2-F9 cells had 72,000 to 77,000 and 40,000 to 48,000 m.w. major components under nonreducing conditions, and had 50,000 to 56,000 m.w. major and 35,000 to 38,000 m.w. minor components under reducing conditions. The 110,000 m.w. component, the third component of IL 2R, was constantly observed in 6H2-F9 hybrid cells.
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PMID:Construction of rat-mouse T cell hybridomas that express regulatable rat interleukin 2 receptor. 309 85

Spleen lymphocytes from C3H/He mice when treated with cisplatin show increased cytostasis and cytotoxicity against Dalton's lymphoma cells in vitro. Cisplatin treatment of splenocytes does not render them cytotoxic/or cytostatic against normal splenocytes. Splenocytes on treatment with cisplatin also produce tumor cell-specific cytotoxic/cytostatic factors (lymphotoxins) which have cytolytic and cytostatic effect on Dalton's lymphoma cells. The increased cytotoxicity of splenocytes on treatment with cisplatin is reversed by the calcium channel blocker nifedipine and the calmodulin antagonist chlorpromazine, suggesting a role of calcium in cisplatin-activated lymphocyte-mediated cytotoxicity.
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PMID:Increased capacity of lymphocytes to lyse tumor cells in vitro and production of lymphotoxins after cisplatin treatment. 326 74

In a study of the biologic consequences of using monoclonal antibodies (mAb) with specificity for I-A for the elimination of an I-A-bearing B cell lymphoma, it was found that, despite the presence of I-A on a number of normal cell types and the propensity of anti-I-A to induce modulation of I-A and I-E on normal cells in vivo, a substantial effect on lymphoma growth could be measured in mAb-treated hosts. Unlike I-A on normal cells, tumor I-A failed to modulate in vivo, and 50% of animals could be cured of lymphoma by multiple doses of anti-I-A mAb. With a sensitive spleen tumor colonization assay, it was shown that neither T lymphocytes nor natural killer cells were involved in tumor elimination by anti-I-A mAb. In addition, C3 depletion only minimally affected the ability of anti-I-A to inhibit tumor growth, suggesting that complement-dependent lysis of tumor cells was not a major mechanism. Spleen cells from long term survivors of tumor challenge and mAb treatment functioned normally as antigen-presenting cells and in the recognition of alloantigens, and serum Ig levels were somewhat higher than in untreated mice; thus, such therapy can be carried out without compromising the immune reactivity of long term survivors.
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PMID:Selective in vivo antitumor effects of monoclonal anti-I-A antibody on B cell lymphoma. 350 Sep 81

We have examined whether pertussis toxin, an agent known to inhibit entry of normal lymphocytes into tissues, affects invasion and metastasis formation by malignant lymphoma and T-cell hybridoma cells. The toxin reduced invasion in vitro in hepatocyte cultures to 20% of control values. Inhibition was maximal after pretreatment for 2 h with approximately 100 ng/ml. The effect of pretreatment with 1 to 5 micrograms toxin/ml for 4 h persisted for at least 5 days, despite a more than 100-fold increase in cell number. The proliferation rate was not affected. Liver metastasis formation after tail vein injection of TAM2D2 T-cell hybridoma cells in syngeneic AKR mice, measured as liver weight, was reduced to 10 to 25% of controls after pretreatment of the cells for 4 h with 1 microgram pertussis toxin/ml. Metastasis to kidneys, ovaries, and lymph nodes was not, or less evidently, affected. With MB6A lymphosarcoma cells no effect was seen after treatment with 1 microgram/ml, but a significant reduction of the liver tumor burden to approximately 50% of controls was achieved by treatment with at least 5 micrograms toxin/ml. Spleen metastasis by MB6A cells was not affected. These results provide evidence for a similarity in invasion mechanisms of normal and malignant lymphoid cells, and they suggest that invasiveness is an important factor in the formation of lymphoma metastases, particularly in the liver.
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PMID:Inhibition of lymphoma invasion and liver metastasis formation by pertussis toxin. 365 46


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