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

Spleen cells from mice bearing methylcholanthrene-induced sarcomas or a mammary adenocarcinoma suppressed the mitogen responses of normal spleen and lymph node cells. Lymph node cells from tumor bearers had no suppressive effects. Centrifugation of spleen cells layered on Hypaque-Ficoll (specific gravity of 1.08) produced a dense fraction which pelleted and a light fraction which was retained at the Hypaque-Ficoll-medium interface. Suppressive activity was not found in either fraction of normal spleen cells. In tumor-bearer spleen cells suppressor activity was greatly enriched in the light fraction. Treatment of the suppressor fraction with anti-theta or anti-Ig serum and complement did not remove suppressor activity. However, the suppressor cells were removed by passage through nylon wool or by carbonyl iron treatment. Also, the population which adhered to plastic Petri dishes contained the suppressor cell activity.
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PMID:Suppressor cells in the spleens of tumor-bearing mice: enrichment by centrifugation on hypaque-ficoll and characterization of the suppressor population. 127 Jul 99

The effect of low dietary zinc on the survival of an intestinal nematode (Heligmosomoides polygyrus) was investigated in two experiments. In experiment 1 (primary infection), outbred CD1 mice were infected once only with 100 H. polygyrus larvae. In Experiment 2 (challenge infection), mice were given a primary infection that was terminated after 9 d using an anthelmintic drug; the mice were reinfected 5 d later. This protocol stimulates host immunity to the second parasitic infection. Three dietary treatments (control, 60 mg Zn/kg diet; zinc-restricted, 5 mg Zn/kg diet; and energy-restricted, 60 mg Zn/kg diet) were used for both experiments. Both infected and uninfected mice were included within each dietary treatment to control for the effect of parasitic infection on host nutritional status. Plasma zinc concentrations were significantly lower in mice fed the zinc-restricted diet, compared with mice fed the control or energy-restricted diets in both experiments; there were no significant differences in plasma alkaline phosphatase activity or tissue zinc concentration. The significant reduction in plasma zinc had no significant effect on worm burden or egg production of H. polygyrus in either experiment, indicating that the 30-40% reduction in plasma zinc was not sufficient to modify parasite numbers. However, the parasite did affect host nutritional status. Spleen weight was significantly higher in infected mice in both experiments. Following the challenge infection, both liver and spleen copper concentrations were significantly higher, and spleen iron concentration significantly lower, in the infected compared with the noninfected mice.
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PMID:Marginal zinc deficiency has no effect on primary or challenge infections in mice with Heligmosomoides polygyrus (Nematoda). 154 14

CRF is a primary integrator of the organism's coordinated neuroendocrine, autonomic, behavioral, and immune responses to stress. In the present study the identity of the cell type(s) expressing CRF receptors in mouse spleen was determined using a combination of cell fractionation and receptor-binding techniques. Autoradiographic studies of the distribution of [125I]Tyro-ovine CRF [( 125I]oCRF)-binding sites in spleen localized CRF receptors primarily to the red pulp and marginal zones. The distribution pattern of [125I]oCRF-binding sites closely resembled the pattern of India ink accumulated in phagocytic cells in the same sections. To identify the specific cell type(s) expressing CRF receptors, [125I]oCRF-binding activity was evaluated in splenic cell populations fractionated on the basis of their physical and functional properties. Macrophages were identified in each fraction by their phagocytosis of polystyrene beads and membrane labeling with MONTS-4, a monoclonal antibody specific for resident macrophages. Spleen cells were fractionated by adherence to glass bead or Sephadex G-10 columns, phagocytosis of carbonyl iron particles, and centrifugation on discontinuous Percoll gradients. By all fractionation methods, there was a significant correlation of [125I]oCRF binding with both phagocytic activity (r = 0.75; P less than 0.001) and MONTS-4 staining (r = 0.84; P less than 0.001), strongly suggesting that CRF receptors are primarily expressed on resident splenic macrophages. However, there was essentially no specific binding of [125I]oCRF to either resident or elicited peritoneal macrophages or to several monocyte/macrophage, B-cell, or T-cell lines. While these results suggest that the expression of CRF receptors may be restricted to a population of splenic macrophages, they do not exclude the possibility that CRF receptors may be induced on resident macrophages in spleen and other immune system-related tissues by factors present in the microenvironment.
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PMID:Corticotropin-releasing factor receptors in mouse spleen: identification of receptor-bearing cells as resident macrophages. 216 23

The antimetastatic activity (AA) of spleen macrophages and T-lymphocytes of mice bearing four syngeneic tumours were tested in adoptive transfer system. Elimination of phagocytic cells by treatment with carrageenan or by carbonyl iron resulted in a complete (tumours LS, MMT1, MMT-T6I) or partial (MMT-T6I) AA decrease. Spleen macrophages (adherent cells) of tumour-bearers possessed a significant AA. The treatment of spleen cells both by anti-Thy-1-serum and by complement enhanced AA of spleen cells of LS and MMT1 tumour-bearers, but led to a partial AA suppression of spleen cells of MMT-T6I tumour-bearers. Thus, the efficiency of antimetastatic defence may considerably depend on the presence of synergism between macrophages and T-lymphocytes in realization of their AA.
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PMID:[Antimetastatic activity of spleen macrophages and T-lymphocytes in mice with transplantable tumors]. 234 23

The effect of in vitro interferon stimulation on nonimmune- and immune-spleen natural killer cell activity was studied in iron-deficient rat pups. Dams were fed 6, 12 or 250 mg Fe/kg diet during gestation and lactation. Approximately one-half of the 17-d-old pups were injected intraperitoneally with 10(5) plaque-forming units of vaccinia virus. Four d later, nonimmune and vaccinia-immune pups were killed. Spleen lymphocyte suspensions were prepared and plated with or without rat alpha/beta interferon for 2 h at 37 degrees C. Washed lymphocytes were combined with 51chromium-labeled YAC-1 target cells and co-cultured for 4 and 16 h at 10 and 50:1 effector-to-target ratios. Hemoglobin concentration, hematocrit, body weight, spleen weight and lymphocyte numbers per spleen were lower in iron-deficient pups than in controls. In general, interferon stimulation increased natural killer cell activity above baseline. Analysis of variance comparison among groups showed that interferon was incapable of restoring natural killer cell activity of iron-deficient pups to the levels observed in control pups. Impaired spleen natural killer cell activity in iron-deficient neonates may be due to a limited capacity for stimulation by interferon.
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PMID:Spleen natural killer cells from iron-deficient rat pups manifest an altered ability to be stimulated by interferon. 246 45

Translational control of ferritin synthesis was studied in rat spleen, and compared with that for liver, heart and brain, in response to iron and inflammation. Spleen concentrations of total RNA in the ribonucleoprotein (mRNP) fraction was comparable to that for liver, while polyribosomal RNA was less. Both fractions were ten-fold lower in heart and brain. In untreated animals, the mRNP fraction of all tissues had the largest portion of the ferritin mRNA, as determined by slot blot hybridization with 32P-labeled cDNA for the L subunit. Acute treatment with ferric ammonium citrate shifted the spleen ferritin mRNA to the polyribosome fraction. This was also so in liver but not in the heart and brain which took up much less iron. The findings were confirmed by hybridization studies of mRNPs and polyribosomes separated in sucrose gradients. Turpentine-induced inflammation also caused a shift in ferritin mRNA from the mRNP to the polyribosome fraction of spleen and liver, over 12 h. We conclude that as in liver, spleen ferritin synthesis is under translational control by iron, and that both tissues also respond to inflammation by shifting of ferritin mRNA to the polyribosomes.
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PMID:Translational regulation of ferritin synthesis in rat spleen: effects of iron and inflammation. 247 Mar 68

Polyunsaturated fatty acids (PUFAs), in the form of pure linoleic, linolenic, or arachidonic acid, were injected subcutaneously into male C57Bl/6 mice daily for 10 days. Injection of 3.6 mg/day of PUFA resulted in up to a two- to threefold increase in spleen weight. Spleen cell response to mitogens was reduced by about 70%; mixed lymphocyte responses were reduced by about 90% when compared to normal values. In admixture experiments, spleen cells from PUFA treated mice suppressed the mitogen induced blastogenic response of control spleen cells by up to 90%. Fractionation of spleen cells from PUFA treated mice by G-10 adherence resulted in an enrichment of suppressive activity in the adherent cells. The suppressive effect of G-10 adherent cells was abolished by the addition of indomethacin as well as by depletion of macrophages by treatments with agents such as carbonyl iron and leucine methyl ester. These studies indicate that the administration of PUFA has marked immunosuppressive effects in mice. These effects may be related to increased prostaglandin production and appear to be mediated by a macrophage type cell.
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PMID:Stimulation of prostaglandin-dependent macrophage suppressor cells by the subcutaneous injection of polyunsaturated fatty acids. 294 62

A second suppressive state (S-SupS) in interferon (IFN) response was demonstrated when mice with third-degree burns of approximately 30% of the body surface area (TI-mice) were stimulated in vivo by Staphylococcal enterotoxin A, a gamma IFN inducer. The first suppressive state in IFN production, appearing 3 to 7 days after thermal injury, was mediated by the generation of splenic suppressor macrophages. The S-SupS was demonstrated approximately 3 weeks post thermal injury. It persisted for almost 3 weeks and gradually disappeared by 7 weeks. Spleen cells from mice during the S-SupS produced less IFN in vitro than normal mouse splenic mononuclear cells (MNC) when stimulated with concanavalin A (Con A). Splenic MNC of mice during the S-SupS inhibited IFN production when they were co-cultured with normal mouse splenic MNC in the presence of Con A. Since this suppressor cell activity could not be removed from TI-mice splenic MNC by carbonyl iron treatment, or by a technique of adherence to a plastic surface, it is suggested that two different cell populations which are capable of suppressing the IFN response of TI-mice exist at different time periods following burn injury.
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PMID:Suppressor cells generated in mice late after thermal injury. 295 4

Spleen cells of chickens infected with IBDV responded poorly to in vitro stimulation with Con A. The mitogenic hyporesponsiveness was due to the presence of suppressor cells that could be removed by pretreatment of IS cells with carbonyl iron or cytodex-3 microcarrier beads. Addition of suppressor cells to normal spleen cells prevented the normal cells from responding to mitogen. Cell-to-cell contact between responder and suppressor cells was not necessary for suppression to occur; the effect was mediated by soluble product(s) released by the suppressor cells. IS cells were also deficient in producing mitogen-induced IL-2 and addition of exogenous IL-2 did not restore mitogenic response of IS.
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PMID:Mechanism of T cell immunosuppression by infectious bursal disease virus of chickens. 303 63

Rats injected with peptidoglycan-polysaccharide polymers derived from group A streptococcal cell walls (PG-APS) develop a chronic, remittant, erosive synovitis. Spleen cells from injected rats failed to proliferate when stimulated in vitro by Con A or PHA, unless nylon wool adherent cells were first removed. The suppression could also be reversed by removing phagocytic cells which had ingested carbonyl iron. Cells from control rats were suppressed in vitro by co-culture with unfractionated or nylon wool-adherent cells from PG-APS injected rats, and the suppressor activity was still expressed after exposure of the suppressor cells to 3,000 rad of irradiation. Addition of catalase and indomethacin to cultures only partially reversed the suppression. T lymphocytes from rats given a single arthropathic dose of PG-APS remained suppressed for at least 86 days after injection. Cells from rats given a low, non-arthropathic dose of PG-APS did not become suppressed. Cells from the Buffalo rat, which is resistant to development of PG-APS-induced chronic arthritis, showed less suppression than cells from the susceptible Lewis and Sprague-Dawley rat strains.
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PMID:Immunosuppressive macrophages induced by arthropathic peptidoglycan-polysaccharide polymers from bacterial cell walls. 306 53


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