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 levels of serum thymic activity (STA), the Thy-1.2 positivity of spleen "spontaneous" rosette-forming cells (SSRFCs) (measured in terms of Az sensitivity), as well as the blastogenic response to specific mitogens for T-lymphocytes, were studied in Balb/C mice after intranasal infection with A/PR/8/34 (HON1) influenza virus. As early as 12 hours, and more drastically, 24 hours the levels of STA were profoundly decreased after virus infection. Spleen Az sensitivity and blastogenic response of thymocytes and splenocytes to stimulation with Concanavalin A and Phytohemagglutinin, respectively, were depressed only later (day 2 or 3). These changes remain evident for about 1 week and later revert to normal values. All of the effects described are dose-dependent and appear to be virus related. Thence the PR8 virus infection initially induces a decrease of STA levels and secondly a impairment of thymus-derived immune functions.
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PMID:PR8 influenza virus infection impairs serum thymic activity levels and thymus-derived immune functions in mice. 286 45

Eleven monoclonal antibodies of rat or mouse origin against the mouse pan T antigen Thy-1 were compared for their ability to reduce mortality from graft-versus-host disease (GVHD) when incubated with donor marrow. Spleen and bone marrow cells were transferred to F1 hybrids or to fully allogeneic (H-2 I-A incompatible) mice. Particular attention was paid to whether complement (rabbit) enhanced the anti-GVHD effect of the antibodies in homozygous histoincompatible chimeras: without complement, 5 IgM anti-Thy-1 and 2 IgG2a anti-Thy-1 did not reduce GVHD. With complement, acute GVHD was completely suppressed. Two of two rat IgG2b anti-Thy-1, however, suppressed acute GVHD without the need for added complement. One of the two also prevented chronic mortality following two haplotype-unmatched transplantation. This antibody, in contrast to other complement-fixing anti-Thy-1 antibodies, had previously been shown to delay rejection of skin allografts. Its specificity did not differ from other complement-dependent Thy-1 antibodies when tested in a cross-blocking radioimmunoassay, and it also had the lower affinity for Thy-1. It seems therefore that only a minority of the antibodies were able to fully exploit the marrow recipients' opsonizing capacity for suppression of GVHD. The important clinical implications of the remarkable difference in immunosuppression of various monoclonal antibodies with comparable specificity and capacity to fix complement in vitro are discussed.
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PMID:Antilymphocytic antibodies and marrow transplantation. VII. Two of nine monoclonal anti-Thy-1 antibodies used for pretreatment of donor marrow suppressed graft-versus-host reactions without added complement. 286 78

A common prediction of clonal deletion/inactivation hypotheses is that cells with high avidity for tolerogen are preferentially eliminated, with low avidity cells being most likely to escape the tolerance induction mechanism. Thus it would be expected that the tolerogen-specific cells in tolerant mice would have a different repertoire than those in normal mice. To find evidence in favor of this prediction, neonatal B10.A mice were rendered tolerant to B10 by the injection of 15 X 10(6) (B10.A X B10)F1 spleen and bone marrow cells, and tolerance was assessed by the acceptance of B10 skin grafts for greater than 50 days. Mice rendered tolerant in this manner contain severely reduced (to less than 10% of normal) but detectable numbers of tolerogen-specific cytotoxic cell precursors that can be activated in the presence, but not absence, of exogenous interleukin 2. Spleen cells from the tolerant animals were compared with those of normal B10.A mice with respect to the expression of differentiation markers on the surface of B10-specific cytotoxic cells and their precursors, and the relative strength of the anti-B10 response toward Kb and Db as a measure of the repertoire of the cytotoxic cell populations. The T cell nature of the tolerogen-specific cytotoxic cells in both normal and tolerant mice was confirmed by their susceptibility to lysis by anti-Thy-1 or Lyt-2 antibody and complement. More importantly, cold target inhibition experiments showed that cytotoxic T cells from tolerant mice were inhibited to a greater degree by B10.A(2R) (KkDb) cold targets than B10.A(5R) (KbDd), suggesting that the response was preferentially directed at the D end of H-2, in direct contrast to normal B10.A spleen cells, which show a preferential response against Kb. Measurement of the frequency of anti-Kb and anti-Db cytotoxic T cell precursors in the spleens of normal and tolerant mice confirmed the differential specificities seen in the cold target experiments. The data suggest that neonatal tolerance induction results in repertoire modification of the anti-tolerogen response rather than a uniform decrease in anti-tolerogen reactivity. Possible mechanisms to explain the alteration in the repertoire of tolerant mice are discussed.
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PMID:Characterization of cytotoxic cells in mice rendered neonatally tolerant of MHC alloantigens: evidence for repertoire modification. 288 56

The effect of injection of a cell homogenate of Trypanosoma gambiense into mice on the production of soluble factors responsible for the induction of polyclonal B-cell activation (PBA) by their spleen cells was examined. PBA was induced by injection of the cell homogenate and was also detected in mice treated with either the serum or the spleen cells of mice treated with the cell homogenate. PBA-inducing activity became detectable in the serum and spleen cells as early as 12 h after injection of the cell homogenate, reached a peak on day 2, and then decreased. This activity was also detected in the culture medium of spleen cells obtained 2 days after injection of the cell homogenate. For determination of the type of spleen cells producing the PBA-inducing factor, the day 2 spleen cells were fractionated on the basis of differences in their adhesive properties. Spleen cells in the effluents from a Sephadex G-10 column (T and B cells) and a nylon wool column (T cells) and those adhering to a plastic flask (macrophages) all produced the PBA-inducing factor. The production of PBA-inducing factor by whole spleen cells and by cells adherent to the plastic flask was not affected by treatment with anti-Thy-1.2 antibody and complement. These data suggest that soluble factors derived from macrophages and T cells could contribute to the induction of PBA. The PBA-inducing activity in the conditioned medium was completely inactivated by treatment at pH 2.0, heating at 56 degrees C for 30 min, or exposure to 0.1% sodium dodecyl sulfate. The results are discussed in relation to cytokines that could affect B-cell activation.
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PMID:Polyclonal B-cell-activating factors produced by spleen cells of mice stimulated with a cell homogenate of Trypanosoma gambiense. 289 May 85

The present study was undertaken to define the cell populations which mediate lymphokine-activated killer (LAK) cell activity in mice. Because old mice exhibit markedly decreased to nondetectable natural killer (NK) cell activity, this age-associated change provided an advantageous system to examine the contribution of NK and T cells to LAK activity. Spleen cells from either young (6-9 weeks) or old (20-26 months) mice were cultured with 1000 units/ml of recombinant interleukin 2 (rIL 2) for 3-5 days. The cells were then tested in a 51 Cr-release assay for their cytotoxicity against NK-resistant fresh tumor cells (MCA-102). The LAK activity exhibited by spleen cells from old mice following 5 days of culture was equivalent to that developed by spleen cells of young mice. This result was contrary to what would be anticipated if mature NK cells comprise the primary precursors of LAK activity, and required further elucidation. The Thy-1 and asialo GM1 (ASGM1) phenotypes of LAK precursor and effector cells were therefore examined by depletion techniques using the appropriate antibodies plus complement. The results using spleen cells harvested after 5 days of culture with rIL 2 showed that LAK effector cells which developed from spleen cells of both young and old mice were predominantly Thy-1+ (85.3% young; 91.8% old) and some coexpressed ASGM1. Spleen cells were treated prior to culture to study the precursor cells. Development of LAK activity by spleen cells from both young and old mice was greatly reduced by pretreatment with anti-ASGM1 plus complement. However, since spleen cells of old mice exhibit very low mature NK activity, these data suggest that the LAK precursors, at least in old mice, may be ASGM1+ NK precursor cells rather than mature ASGM1+ NK effector cells. In addition, treatment with anti-Thy-1 plus complement inhibited generation of a significant proportion of LAK activity only in the spleens of old mice, suggesting a qualitative difference in LAK precursor cells with age and supporting the heterogeneity of the cells which are capable of developing LAK activity.
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PMID:Lymphokine-activated killer cells and aging in mice: significance for defining the precursor cell. 289 85

Effects of carrageenan (CAR) treatment on the response of interferon (IFN) production in vivo and in vitro after stimulation with an IFN-gamma inducer, staphylococcal enterotoxin A (SEA), was investigated. The IFN-gamma production in mice stimulated with SEA was impaired after i.v. administration of a 20 mg/kg dose of CAR. Spleen cells (SC) from CAR-treated mice had decreased ability to produce IFN in vitro after stimulation with the same inducer. SC obtained from mice during the suppressive state inhibited IFN-gamma production when they were co-cultured with mononuclear cells prepared from spleens of untreated control mice. This suppressor cell activity could be removed from SC by an adherence technique to plastic surface. The SC with suppressor activity were not inactivated by treatments with monoclonal anti-Thy-1.2 antibody, anti-asialo GM1 antisera and anti-mouse immunoglobulin antisera followed by complement. The suppressive activity was detected in cell-free culture fluids of macrophage fractions containing suppressor cell activity. These results suggest that the decrease in IFN-gamma production in mice pretreated with CAR may associate with the presence of suppressor cells characterized to the monocyte/macrophage lineage.
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PMID:Suppression of interferon gamma production in mice treated with carrageenan. 293 70

We examined whether C5-sufficient mice which are naturally tolerant to this antigen have suppressor T cells to C5 humoral immune response. Two congenic strains of mice B10.D2 (NSN) and B10.D2 (OSN) differing only in the presence or absence of C5 were used. Irradiated (760 rds) sufficient hosts were reconstituted with a nonadherent spleen cell suspension from either sufficient or deficient mice or a mixture of both. Hemolytic C5 levels were assayed. Sufficient spleen cells appeared to prevent the drop of C5 level caused by anti-C5 antibody made by deficient spleen cells. Spleen cell suspensions from sufficient mice primed with deficient spleen cells exhibited better anti-C5 activity than normal sufficient spleen cell suspensions. This anti-C5 activity is abrogated by treatment of the NSN spleen cell suspensions obtained from NSN primed with OSN spleen cells with anti-Thy-1.2 antiserum and complement. Suppression of the humoral response to C5 failed to affect the anti-sheep red blood cell immune response. Suppressor T cells are resistant to low-dose irradiation, cortisone treatment and adult thymectomy. In contrast, they are sensitive to high doses of irradiation and both high and low doses of cyclophosphamide treatment. Thus, C5-sufficient mice, in contrast to C5-deficient mice, appear to have antigen-specific suppressor T cells which downregulate the humoral immune response to C5. In addition, we examined the relationship of these suppressor T cells to the state of tolerance in helper T cells of C5-sufficient mice. This was done in irradiated deficient mice which were repopulated with spleen cell suspensions selectively depleted of either Lyt-1+ or Lyt-2+ T cell subsets. These chimeras were challenged with murine C5 and both the primary and secondary immune response was measured by inhibition of the C5 hemolytic activity. It was found that only spleen cell suspensions of the deficient mice selectively depleted from the Lyt-2+ subset of T cells responded to the antigen both in the primary and secondary response. In contrast, either subset of T cells from the sufficient mice failed to respond. Thus, it appears that in sufficient mice helper T cells to C5 are intrinsically tolerant or physically and/or functionally deleted. In conclusion, the data suggest that both T cell compartments are unresponsive and play a role in the mechanism of tolerance to a physiologic antigen.
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PMID:Mice naturally tolerant to C5 have T cells that suppress the response to this antigen. 294 29

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

Spleen cells from B6D2F1 hybrid mice pretreated with 5 X 10(7) B6 spleen cells iv 7 days earlier (B6-pretreated B6D2F1) exhibit a reduced capacity to stimulate the in vitro proliferative and anti-D2 CTL responses of B6 spleen cells. This inability of B6-pretreated B6D2F1 spleen cells to stimulate B6 spleen cells efficiently is due neither to the absence of stimulating cells bearing the D2 alloantigens nor to the destruction of B6 responding cells, but to the presence in the B6-pretreated B6D2F1 cell population of a suppressor mechanism, since the addition of B6-pretreated B6D2F1 spleen cells to a culture of normal B6 responding and irradiated B6D2F1-stimulating spleen cells can suppress the B6 anti-B6D2F1 response. This suppression is mediated by a nylon adherent, Thy-1-negative cell of parent-strain origin which is radioresistant at 2000 R. This suppressor cell is not induced by the injection to B6D2F1 hybrids of spleen cells from the other parent strain (D2) or an allogeneic strain (C3H). It does not suppress either the response of the other parent (D2) or an allogeneic strain (C3H) to B6D2F1 antigens, or the response of B6 cells to an allogeneic strain (C3H).
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PMID:Specific suppression of the in vitro parent anti-hybrid reaction. I. Characterization of a suppressor cell induced in hybrids by pretreatment with parent-strain spleen cells. 294 55

To clarify the immunopharmacological action of an extract isolated from inflamed skin of rabbits inoculated with vaccinia virus (Neurotropin), its effect on delayed type hypersensitivity (DTH) response to sheep red blood cells (SRBC) in mice was examined. Neurotropin enhanced the DTH response in C57BL/6 mice which were low responders to SRBC, but not in either BALB/c or C3H/He mice (high responders) when administered i.p. for 4 consecutive days prior to sensitization. However, Neurotropin did not affect the formation of plaque-forming cells to SRBC in C57BL/6 mice under the condition where it enhanced the DTH response. We further examined the mechanism by which Neurotropin enhanced the DTH response in C57BL/6 mice by means of cell transfer experiments. Spleen cells from mice administered Neurotropin i.p. for 4 days, but not saline, could enhance the DTH response when transferred i.v. into normal syngeneic mice just before sensitization. However, the treatment of the spleen cells with anti-Thy-1.2 + complement (C) or with anti-Lyt-1.2 + C, but not with anti-Lyt-2.2 + C, abrogated its enhancing effect. The depletion of macrophages from the cells had no effect. On the other hand, the spleen cells from mice administered Neurotropin had no enhancing effect in the effector phase of DTH response, and they showed a helper T cell activity in a DTH helper T cell assay system in which cyclophosphamide-treated mice were used as recipients. These results suggest that Neurotropin enhances the DTH response in low responder mice through the induction of Lyt-1+2- DTH helper T cells.
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PMID:Immunopharmacological actions of an extract isolated from inflamed skin of rabbits inoculated with vaccinia virus (neurotropin); enhancing effect on delayed type hypersensitivity response through the induction of Lyt-1+2- T cells. 295 31


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