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)

The late effects of various immunosuppressive insults on cell-mediated immunity in mice were studied in an attempt to assess the role of immune surveillance in the aging process. Results were obtained using susceptibility to allogeneic tumor cell challenge, graft-versus-host reaction (GVHR), blastogenic response to PHA, a thymus derived T cell-specific plant mitogen, and cytolytic activity against allogeneic tumor cells as measures of immunologic activity. In vivo studies late in life show that resistance to allogeneic tumor cells is significantly decreased in thymectomized mice, whereas those treated with cortisone, cyclophosphamide and sublethal X-ray remain unchanged. Spleen cells from only the thymectomized and the sublethally irradiated mice show reduced activity in the GVHR. No difference is seen in the activity of bone marrow cells. Results consistent with these findings were obtained in in vitro studies. Thus spleen cells from thymectomized or sublethally irradiated mice show decreased activity is response to PHA, whereas no change is seen in spleen cells from other treated groups. Hence, surgical and physical insults are more likely to induce long-lasting immunosuppression in those immunocompetent tissues whose activity normally diminishes with advancing age. Furthermore, the degree of immunosuppression seen in this study is not of the order of magnitude that one could reasonably predict a significant decrease in mean life-span.
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PMID:The late effects of selected immunosuppressants on immunocompetence, disease incidence, and mean life-span. II. Cell-mediated immune activity. 0 May 62

It was established that intracerebral introduction of 10 min parental cells of the spleen brought about in hybrids (CBAXC57Bl/6) F1 infiltrative-destructive changes (development of lymphocytic infiltrations, dystrophy in the nerve cells, myelin fibres and neurogliacytes) the intensity of which was found to be considerably higher in cases of injection of parental spleen cells from specifically sensitized donors. Spleen cells of mice CBA produced much greater changes as compared with those produced by spleen cells of mice C57Bl/6. Inoculation into the mice brain of 10 mln of spleen cells together with tumour in a dose of 1500 cells produced a clear cut inhibitory effect on the tumour growth, this effect being more pronounced following introduction of sensitized cells of the spleen of mice CBA.
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PMID:[Morphological manifestations and morphogenesis of the graft vs. host reaction in the brain of F1 hybrids following the administration of parental lymphoid cells and its effect on tumor inoculation]. 0 Sep 84

The immunological unreactive state occurring in (T,G)-A-L nonresponder mice after secondary antigen challenge was investigated. Syngeneic IgM anti-(T,G)-A-L antibody-containing plasma, transferred at the time of the time of primary challenge, induced persistent suppression of autologous specific antibody production. Removal of plasma IgM with goat anti-mu antisera removed the ability of the plasma to supress. The induction and maintenance of the suppressed state were not different in thymectomized or sham-thymectomized animals. Primed animals subjected to graft-vs-host reaction (GVHR) at the time of secondary challenge switched over to IgG production. Animals suppressed by passive antibody transfer reacted to GVHR, at the time of secondary challenge, with specific IgM but not IgG antibody production. Transfused normal spleen cells partially abrogated suppression only when (suppressed) hosts had been lethally irradiated. Spleen cells from antigen-plus-antibody suppressed donors, upon transfer to previously normal, syngeneic hosts, were less immunocompetent than spleen cells from untreated donors. These data are consistent with a model of IgM mediated, T cell-independent persistent suppression of humoral immunity.
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PMID:IgM-mediated, T cell-independent suppression of humoral immunity. 0 7

Treatment of DBA/2 (H-2d) mice with bacterial endotoxin prior to transplantation of their spleen and lymph node cells into immunosuppressed AKR (H-2k) mice prevented acute mortality from graft-versus-host (GVH) disease. AKR mice that received immunocompetent cells from untreated DBA/2 mice had a median survival time (MST) of 13 days. In contrast, AKR mice that received immunocompetent cells from endotoxin-treated DBA/2 donors had an MST of 54 days. Endotoxin treatment of AKR recipients was not essential for preventing mortality from acute GVH disease. Chimerism was proved by demonstrating that the lymphoid cells of long-term surviving AKR mice had the characteristics of DBA/2 lymphoid cells as measured by their response in mixed leukocyte culture (MLC) tests. Spleen cells from endotoxin-treated DBA/2 mice were able to stimulate, and to be stimulated by, AKR spleen cells in MLC assays. Furthermore, spleen cells from endotoxin-treated DBA/2 mice did not suppress the responses of DBA/2 or AKR spleen cells in 'three-party' MLC tests.
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PMID:Mitigation of graft-versus-host disease in mice by treatment of donors with bacterial endotoxin. 0 35

Murine spleen cells were separated on the basis of adherence to glass beads into distinct subpopulations that differ in their ability to produce acute graft-versus-host disease (GVHD). Nonadherent CBA spleen cells produce acute GVHD in 6-10 days in lethally irradiated (C57BL/6 X CBA)F1 mice as do unfractionated spleen cells. Spleen cells which are adherent to glass beads, however, enable 71% of the mice to survive without symptomatology of acute GVHD. The low proliferative response of these cells to phytohemagglutinin (PHA) correlated with the mitigated GVHD seen in animals grafted with this fraction. Proliferative cells as determined by the spleen colony assay and the in vitro agar colony-forming assay are present in this fraction as are cells responsive to mitogenic stimulation with lipopolysaccharide (LPS). B6CBF1 mice grafted with CBA adherent cells exhibit a gradual return over a period of 5 months to normal PHA and LPS stimulation levels as shown by splenic cell responses of these mice to mitogens. Surviving mice grafted with adherent cells were chimeric as determined by electrophoretic hemoglobin pattern analysis and serial bone marrow transplantation.
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PMID:Mitigation of graft-versus-host disease in lethally irradiated mice grafted with spleen cells adherent to glass beads. 0 63

Immunological tolerance to Gross virus-specific transplantation antigens in rats given neonatae transfer of donor lymphoid cells beneath the kidney capsule of syngeneic recipient rats. Immune or normal donor cells invariably developed a cell-mediated immune reaction in kidneys of GV-tolerant recipients, presumably against GV antigens present on the surface of recipient lymphoid cells in the kidney. Spleen and lymph node cells from tolerant rats failed to develop a reaction in tolerant recipients, but developed a strong reaction to histoincompatible antigens in the kidneys of semisyngeneic tolerant rats. The immunologically tolerant state in the rats could be broken by adoptive transfer of spleen and lymph node cells from syngeneic rats immunized with GV-induced lymphoma cells. Immunotherapy of a GV-induced and also a GV-infected methylcholanthrene-induced fibrosarcoma growing in tolerant rats was successful when immune spleen and lymph node cells were administered i.p. 3 days after s.c. inoculation of 2 X 10(7) tumor cells in the case of the lymphoma, and 1 day after inoculation of 5 X 10(6) tumor cells in the case of the fibrosarcoma.
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PMID:Adoptive immunotherapy of a Gross virus producing lymphoma and a methylcholanthrene-induced fibrosarcoma in tolerant rats. 1 76

Spleen cells from BALB/c mice primed with keyhole limpet hemocyanin (KLH), were stimulated with heat-killed vaccine of rough Pneumococcus pneumoniae R36A (Pn) and/or phosphorylcholine (PC)-coupled KLH to induce an anti-PC response in vitro. The response to PC-KLH was found to be T-dependent while it is T-independent to Pn. The antibodies induced with either antigen had similar avidity and expressed the TEPC 15 idiotype exclusively; thus T cell involvement in the response to PC-KLH failed to alter these parameters of the anti-PC response. At the precursor cell level, Pn induced small clones with an average size of 10 plaque-forming cells (PFC), whereas PC-KLH gave rise to larger clones of 40-50 PFC. This difference in the proliferative potential of PC precursor B cells hinted at the possibility that Pn and PC-KLH were stimulating different precursors. This was corroborated by the observation that a) when Pn and PC-KLH were added to the same cultures a synergistic effect was seen, i.e. the number of plaques was greater than the sum of the responses induced by each antigen, and b) in microcultures, under conditions limiting B cells only, Pn plus PC-KLH induced a higher fraction of responding wells than either antigen on its own. We postulate that Pn and PC-KLH stimulate subpopulations of PC precursor cells which are T-independent and T-dependent, respectively.
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PMID:Antibody response to phosphorylcholine in vitro. II. Analysis of T-dependent and T-independent responses. 1 Nov

The local graft-versus-host reaction as evaluated by the popliteal lymph node enlargement was used for studying the immunosuppressive potency of placental steroid 5alpha-androstane-3,17-dione. Spleen cells from virgin female mice and rats injected subcutaneously with this steroid compound produced in appropriate F1 recipients a significantly weaker reaction (P less than 0.001) than spleen cells from untreated or medium-treated control animals. On the other hand, the pretreatment of cell donors either with 5beta-androstane-3,17-dione or testosterone, the compounds which are not present in the mouse and rat placenta, did not influence the normal graft-versus-host reactivity.
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PMID:Reduction of the graft-versus-host reactivity of mouse and rat spleen cells by 5alpha-androstane-3,17-dione. 1 Nov 36

Bone marrow cells (0,5-10(6)) of female mice of CBA or C57BL strains were injected intravenously to lethally irradiated CBA, C57BL/6, (femaleCBA X maleC57BL/6)F1 and (femaleC57BL/6 X maleCBA)F1 mice. Spleen of recipients as assayed for colony count on the 9th day after bone marrow transplantation by the method of Till and McCullouch. Stem cells of CBA mice demonstrated failure of allogenic inhibition in (CBA X C57BL/6)F1 hybrid mice and formed the same number of colonies as in the spleen of syngenic recipients. The level of allogenic inhibition of CBA stem cells transplanted to (C57BL/6 X X CBA)F1 hybrid mice was 50%. Bone marrow cells of C57BL/6 mice formed colonies in spleen of (CBA X C57BL/6)F1 mice at least in 20 times less than in syngenic combination. In the transplantation of bone marrow from C57BL/6 mice to (C57BL/6 X CBA)F1 hybrid mice the allogenic inhibition was less pronounced (77-85%) as compared with the transfer of cells to (CBA X C57BL/6)F1 hybrid mice (95%). The sex of a recipient did not influence the number of formed colonies. The different level of allogenic inhibition of parental stem cells can not be explained by the effect of linkage with sex as the female of reciprocal hybrid mice have identical structure of sex chromosomes (X(CBA)XC57BL/6). The data obtained indicate that the maternal effect affects allogenic inhibition of stem cells in parent--F1 system. It is possible that the maternal influence may be determined by cytoplasmic factors of inheritance which affect the expressivity of recessive genes Hh, controlling the inheritance of specific haematopoietic cell antigens.
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PMID:[Influence of the maternal effect on allogenic inhibition of hematopoietic stem cells]. 1 Nov 51

Spleen cells from (CBA X C57/BL) F1 mice undergoing graft-versus-host (GVH) reaction induced by injection of parental cells 7-14 days previously are capable of suppressing an immune response by normal or primed F1 spleen cells to chicken erythrocytes and levan in vivo and sheep erythrocytes in vitro. The cells in these GVH spleens which were responsible for the suppression were sensitive to treatment with anti-0 serum, resistant to 900 rad irradiation in vivo and not retained by anti-immunoglobulin columns. Suppressor activity in vitro was present only in the non-adherent fraction of these GVH cell suspensions. Furthermore, the T-cell fraction, purified by affinity chromatography, suppressed the in vitro response of macrophage-depleted normal F1 cells to DNP-levan. Collectively, these observations imply that suppressor T cells generated by GVH reaction can affect B-cell functions directly without intermediary macrophage participation. Spleen cells from (CBA X C57/BL) F1 mice undergoing GVH reaction induced by C57/BL cells were depleted of their F1 content by treatment with anti-CBA alloantiserum. The suppressive activity of the residual donor component was still expressed against other F1 cells (AKR X C57/BL) which were H-2 compatible with the original host, but not against H-2-incompatible cells (DBA/1 X C57/BL) F1. However, the latter were suppressed in the presence of (CBA X C57/BL) F1 cells. Thus, interaction of donor T cells with F1 target cells containing those H-2 antigens towards which they are sensitized is mandatory for the subsequent manifestation of immunosuppressive activity. GVH cells suppressed the response of primed F1 cells in double Marbrook chambers when the two populations were separated were by a cell-impermeable membrane, provided the GVH suspension contained F1 cells to which donor T cells were sensitized. This suggests that soluble factors are involved in the mechanism of GVH-induced immunosuppression.
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PMID:Analysis of immunosuppression generated by the graft-versus-host reaction. II. Characterization of the suppression cell and its mechanism of action. 1 Nov 81


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