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

By use of 99mTc-sulfur colloid, splenic size as well as liver/spleen ratio of ratioactivity was determined after external radiation of the abdomen. In six patients receiving about 2,000 R whole-abdominal radiation, there was no atrophy of the spleen or abnormal distribution in the liver/spleen ratio of radioactivity (that is, the spleen was still functional). Serial studies in a 7-year-old boy with acute lymphoblastic leukemia in remission showed that 1,450 R splenic radiation did not result in any appreciable change in the length of the organ. In a woman with lymphosarcoma, a change in spleen size did not occur until a dose of 1,800 R was delivered. Another patient had apparently normal uptake of radiocolloid 5 years after 3,600 R. Hence the normal spleen and the spleen affected by other diseases may be far more resistant to external radiation than the spleen diseased with chronic myelocytic leukemia. Spleen scans can be useful in documenting the response of the organ to radiation.
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PMID:Radiocolloid scans in evaluating splenic response to external radiation. 16 50

We examined the effect of rotation-induced stress on (1) growth of lymphosarcoma tumors; (2) interleukin-2 (IL-2) production; (3) T cell subset distribution; and (4) cytotoxic T cell (CTL) function. In addition, we examined the levels of corticosterone and beta-endorphin as possible mediators of stress-induced immune alterations. Rotation stress induced progressive lymphosarcoma growth, while unstressed mice showed tumor regression after 2 weeks of growth. IL-2 production and CTL activity in stressed animals were significantly lower than controls during the first 2 weeks after initiation of stress. Spleen lymphocytes from stressed and control mice bearing the L3T4 antigen (helper/inducer T cell marker) remained unchanged, while in peripheral blood such cells decreased in stressed but not control animals. This latter pattern was also observed in Lyt 2 positive (suppressor/cytotoxic) cells of both spleen and peripheral blood. Corticosterone levels were elevated for an extended period following initiation of stress, while beta-endorphin levels remained similar to those of the controls. Although these data do not directly establish a causal link between immunoinhibition and tumor growth, they clearly demonstrate that stress inhibits a number of cell-mediated immune functions that may be relevant in this regard.
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PMID:Stress-induced decline in immune responsiveness in C3H/HeJ mice: relation to endocrine alterations and tumor growth. 326 57

DBA/2 mice were immunized i.p. against syngeneic SL2 lymphosarcoma cells. At various days after the last immunization peritoneal and spleen lymphocytes were collected. The lymphocyte suspensions were enriched for T-cells by nylon wool filtration. The peritoneal T-cells from immunized mice (a) expressed direct specific antitumor cytotoxicity in vitro, (b) induced macrophage cytotoxicity in vitro, and (c) exerted tumor neutralization measured in a Winn-type assay. Spleen T-cells from these immunized mice (a) expressed no direct specific antitumor cytotoxicity in vitro, (b) only induced moderate macrophage cytotoxicity in vitro, but (c) exerted tumor neutralization in a Winn assay. For effective tumor neutralization in vivo effector target cell ratios of 1000:1 were required. When the effector/target ratio of 1000:1 was maintained but the absolute numbers of effector and target cells were lowered from 10(6) to 10(5) lymphocytes and 10(3) to 10(2) target cells respectively, no tumor neutralization was obtained. The major effect of the sensitized-transferred T-lymphocytes seemed to be the induction of cytotoxic macrophages in the (naive) recipient mice, as the peritoneal macrophages collected from the recipient mice 7 days after i.p. injection of a mixture of sensitized T-cells and tumor cells were cytotoxic. Purified peritoneal T-lymphocytes collected from these recipient mice were able to induce macrophage cytotoxicity in vitro but expressed no cytotoxic T-cell activity. In conclusion, our results show that in the tumor system used, tumor neutralization after transfer of sensitized lymphocytes is not dependent on the presence of cytotoxic T-lymphocytes. Lymphocytes with the strongest potency to render macrophages cytotoxic (in vitro and in vivo) also induce the best tumor neutralization in vivo, suggesting an important role for host macrophages as antitumor effector cells.
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PMID:The role of host lymphocytes and host macrophages in antitumor reactions after injection of sensitized lymphocytes and tumor target cells into naive mice. 353 93

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

The ontogenesis of the bovine immune response was studied in three embryos (<40 days) and 106 fetuses of various ages. In the absence of overt antigenic stimulation, fetuses had lymphoid development of the thymus at 42 days of gestation, the spleen was structurally present at 55 days, and certain peripheral lymph nodes were present at 60 days. Mesenteric lymph nodes were structurally present by 100 days of gestation, and lymphoid tissue of the gastrointestinal tract, particularly the lower ileum, was observed in histologic sections of a 175-day fetus with a bacterial infection. Pyroninophilic cells, plasma cells, and germinal centers were present in lymph node sections of antigenically stimulated fetuses. Lymphoid tissue developed more rapidly in fetuses with bacteria, viral antigens, or apparent maternal red-blood-cell antigens than in the normal fetus. Thymic and splenic indices reached maximal values in the 205- to 220-day fetal age group. Immunoglobulin M (IgM)-containing cells were first observed, by immunofluorescence, in a single fetus at 59 days of gestation. Immunoglobulin G (IgG)-containing cells were observed at 145 days of gestation in one fetus with a bacterial and viral infection. IgM-containing cells were observed in 36 fetuses and IgM and IgG cells were present in seven fetuses. Spleen, lymph nodes, thymus, bone marrow, and liver of one fetus from a dam with lymphosarcoma had immunoglobulin-containing cells. Hemal lymph nodes, blood (buffy coat), Peyer patches, and heart and lung sections from fetuses with immunoglobulin-containing cells in spleen or lymph node did not have immunoglobulin-containing cells. Antigens of the virus of bovine virus diarrhea-mucosal disease (BVD) were detected in one fetus, and antigens of infectious bovine rhinotracheitis (IBR) virus were detected in three fetuses; however, viruses were not isolated in primary bovine embryonic kidney cells. Two of the three fetuses with IBR virus antigens had neutralizing serum antibody titers to IBR virus. Bacteria including Escherichia coli, Lactobacillus sp. and Mima polymorpha var. oxidans were isolated from four fetuses. Antibodies that caused the agglutination of maternal red blood cells were present in 8 of 20 bovine fetal serum samples. The antibodies were 2-mercaptoethanol sensitive and partially heat resistant (56 C for 30 min). The ontogeny of the bovine immune response and human immune response were compared, and it was suggested that the similarities were primarily due to the two species having the same approximate gestation period of 280 days.
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PMID:Ontogeny of the bovine immune response. 412 77

Spleen cells sensitized to tumour cells have an anti-tumour effect on injected syngeneic lymphosarcoma cells in mice. This study shows that this anti-tumour effect can be enhanced by induced peritoneal macrophages and by macrophage-like tumour cells (macrophages). Addition of macrophages to the intraperitoneally injected sensitized spleen cells stimulated the anti-tumour effect. This was observed both with intraperitoneally injected tumour cells and with subcutaneously transplanted tumour cells. The anti-tumour effect is the result of a cooperation between T cells and macrophages. In vitro incubation of immune T-cells with macrophages or macrophage-like cells enhanced the in vivo anti-tumour activity of the sensitized T-lymphocytes. Neither the presence of antigen nor the proliferation of the immune T-cells were a prerequisite to enhance this anti-tumour effect. Our experiments suggest that a macrophage factor is responsible for the enhancement of the anti-tumour effect. Based on the results of this paper and other studies we propose the following sequence of events to explain the anti-tumour effect of injected sensitized T-lymphocytes and macrophages: injected macrophages enhance the anti-tumour effect of sensitized lymphocytes. These stimulated lymphocytes migrate to the tumour located elsewhere and recognize the tumour antigens. Subsequently, the lymphocytes render (host) macrophages in the tumour cytotoxic to tumour cells.
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PMID:A macrophage factor enhancing the systemic anti-tumour effect of T lymphocytes. 660 76

Cystatin C is the best known extracellular endogenous cysteine proteinase inhibitor and has been studied as a possible index of tumor growth and as a marker of the effectiveness of antitumor therapy. The aim of this study was to evaluate cystatin C concentrations in murine tumor tissues (compared with other organs not directly involved with tumor development, such as the liver and spleen) during treatment with several antitumor drugs (Ukrain and/or cyclophosphane). Cystatin C concentrations in murine tissues and biological fluids was determined by enzyme-linked immunosorbent (ELISA) assay. The cystatin C ELISA test is a sandwich immunoassay, which uses immobilized rabbit antihuman cystatin C Pab and mouse antihuman cystatin C Mab-HRP (monoclonal antibodies, conjugated with horseradish peroxidase). We observed decreased serum cystatin C concentrations compared with controls in all nontreated tumor models: HA-1 hepatoma (solid and ascitic forms), lung adenocarcinoma (solid and ascitic forms) and LS lymphosarcoma. In the ascitic fluid of mice with HA-1 hepatoma the cystatin C concentration was much lower than in the serum of the same mice (about 20-fold lower). In the HA-1 model of hepatoma cells cystatin C concentration decreased about 2-3-fold compared with the control (intact liver) and Ukrain significantly increased the cystatin C concentration. Cyclophosphane treatment of LS lymphosarcoma significantly increased the cystatin C concentration in serum. Cyclophosphane treatment (50 mg/kg, single injection) increased cystatin C by up to 8-fold more in tumor issue. Ukrain treatment of LS lymphosarcoma was also followed by increased levels of cystatin C in tumor tissue (4-fold); cyclophosphane plus Ukrain had a similar positive effect. In the group with LS lymphosarcoma Ukrain or cyclophosphane plus Ukrain treatment induced a significant increase in cystatin C concentration in liver. Liver cystatin C concentration decreased in the HA-1 hepatoma group and treatment with Ukrain or carboxymethylated beta-1, 3-glucan (CMG) increased this index in both groups. Spleen cystatin C concentrations decreased about 5-fold in LS lymphosarcoma compared with controls and combined treatment with cyclophosphane plus Ukrain restored the index to the normal value. We can conclude that both murine tumors studied were characterized by low cystatin C concentrations in tumor tissues and decreased cystatin C concentrations (to a lesser degree) were also observed in liver and spleen as a result of the "toxic" effect of tumor bearing. Effective treatment in all cases (especially with Ukrain or a combination of cyclophosphane plus Ukrain) induced a significant increase in cystatin C. Obviously, the decrease in cystatin C concentration predominantly in tumor tissue was connected with tumor development and restoration of cystatin C level may be used as a marker of efficacy of antitumor therapy.
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PMID:Cysteine proteinase inhibitor level in tumor and normal tissues in control and cured mice. 1134 42