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)

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

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

Spleen and lymph node cells from DBA/2 (H-2d) donor mice treated with multiple injections of bacterial lipopolysaccharide (LPS) were tested in vivo for reactivity against normal tissues of host AKR (H-2k) mice against an AKR long-passage, acute lymphoblastic leukemia (BW5147). LPS treatment of donor mice resulted in a reduction in graft-versus-host (GVH) reactivity without loss of graft-versus-leukemia (GVL) reactivity. Immunocompetent cells from LPS treated DBA/2 donors were effective when used for adoptive immunotherapy (in combination with chemoradiotherapy) of BW5147 leukemia. GVH associated mortality decreased as the dose of spleen cells from LPS treated histoincompatible donors was increased as much as four times the number necessary to eliminate leukemia. The mechanism by which LPS reduced GVH reactivity without eliminating GVL reactivity is unclear; however, it does not appear to be the result of a dilution in the number of GVH reactive cells by nonlymphoid elements in the donor spleen nor of the adjuvant effects of LPS on resistance to bacterial infections.
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PMID:Graft versus leukemia. VIII. Selective reduction in antihost reactivity without loss of antileukemic reactivity by treatment of donor mice with lipopolysaccharide. 2 84

The influence of cholera toxin (CT), and thus probably of cyclic AMP, on the capacity of parental lymphoid cells to elicit a graft-versus-host reaction (GVHR) was studied. Toxin-treated DBA/1 mice were used as cell donors and untreated DBA/1xC57B1/6 F1 hybrid mice as recipients, and the GVHR reactivity of the transferred cells was estimated by their ability to induce spleen enlargement or stimulation of antibody formation ('allogenic effect') in the recipients. Spleen cells from donors intravenously injected with 1 microgram CT 1-3 days earlier, gave a significantly stronger GVHR than did spleen cells of untreated mice. Choleragenoid, a toxin analog devoid of the toxin's ability to activate plasma membrane adenylate cyclase even though it binds efficiently to cells, had no effect on the GVHR-inducing capacity of the spleen cells. The enhanced GVHR by spleen cells from toxin-treated DBA/1 animals was reduced to the normal level when the donor cells were transferred along with lymphoid cells from untreated animals of the same strain. Spleen was the most powerful source of the suppressive influence. No evidence for a redistribution of suppressor cells following administration of CT was found. Spleen cells from mice syngeneic with the recipients had no suppressive effect. The results suggest that parenterally administered CT, directly or indirectly, can inhibit a cell population in spleen which normally exerts an antigen-specific suppressive regulatory influence on the development of GVHR.
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PMID:Interaction of cholera toxin and toxin derivatives with lymphocytes. III. Modulating effects in vivo by cholera toxin on the graft-versus-host reactivity of lymphoid cells: suggested inhibition of suppressor cells. 2 37

The X-chromosome-linked B lymphocyte defect of CBA/N mice has been studied in vitro by comparing the ability of (CBA/N X DBA/2)F1 (X-/X- X X+/Y) male (X-/Y) and female (X-/X+) spleen cells to respond to the thymus-independent antigen DNP (or TNP)-AECM-Ficoll. (CBA/N X DBA/2)F1 male spleen cells failed to generate significant in vitro anti-TNP antibody responses to DNP- or TNP-AECM-Ficoll, in contrast to spleen cells from F1 female (X-/X+) mice which responded normally to these T-independent antigens. Spleen cells from male F1 mice responded almost as well as F1 female cells to the thymus-dependent antigen, TNP-sheep red blood cells (TNP-SRBC) in vitro. Adding F1 male cells to F1 female cells failed to reduce the response of the latter to DNP-AECM-Ficoll, suggesting that the inability of F1 male cells to respond was not due to active suppression. The response of F1 male spleen cells to TNP-SRBC was not impaired by adding high concentrations of TNP-AECM-Ficoll indicating that the mechanism of unresponsiveness was not tolerance induction in all TNP-specific precursors. Lymphocytes from F1 male mice were capable of forming anti-TNP antibody after stimulation with lipopolysaccharide (LPS) in high concentrations; DNP-AECM-Ficoll had no effect on this polyclonal response. B lymphocytes from mice bearing only the X-chromosome of the CBA/N strain thus display a profound defect in B cell activation. This functional defect may represent either an inability of the defective B cells to be activated by thymus-independent antigens or the absence of a sub-class of B cells which respond to thymus-independent antigens.
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PMID:In vitro studies of the genetically determined unresponsiveness to thymus-independent antigens in CBA/N mice. 5 35

Mice were irradiated, infused with thymocytes and immunized with a variety of antigens, i.e., sheep or horse red blood cells (SRBC or HRBC), diphtheria toxoid (DT) or bovine gamma-globulin (BGG). The spleen cells (T.Spleen cells) were harvested 5 days later and cellfree extracts were prepared. The extracts contained an allogeneic suppressive factor (ASF) that was capable of inhibiting IgM antibody responses of allogeneic or semi-allogeneic unirradiated mice. ASF had to be injected within 24 hr of immunization to be effective and a single injection delayed, rather than abolished, the antibody response at the cellular level. However, daily injections of ASF resulted in persistent suppression of antibody response. ASF activity was antigen nonspecific, i.e., the antigen used to stimulate ASF production did not have to be the same as the antigen used to test for ASF activity. C3H T.Spleen extracts were even immunosuppressive when prepared by exposure to C3BF1 alloantigens only; such extracts suppressed antibody responses of C3BF1 and DBA/2 mice. C3H ASF was removed from extracts after incubation with C3BF1 spleen cells but not after incubation with C3H spleen cells. C3BF1 spleen cells which had been preincubated with C3H ASF were unable to generate antibody-forming cells upon transfer to irradiated C3BF1 host mice. This suggests that the ASF molecule may be or include receptors for alloantigens. The immunogenetic requirements for ASF activity were evaluated by injecting extracts from C3H, C57BL, C3BF and BALB/c T.Spleen cells into C3H, CBA, C57BL, BALB/c, DBA/2, A or C3H.A recipient mice. All extracts tested had ASF activity. However, all allogeneic recipients were not suppressed by the extract material. The suppressive activity of ASF seemed to require two (or more) antigenic differences between donors and recipients of extract material, an H-2K or I antigen difference and a second antigen difference, possibility Ig-1. In the limited numbers of strain combinations tested, T.Spleen extracts suppressed IgM antibody response only if exposed to H-2 and Ig-1 antigens, e.g., BALB/c (H-2d, Ig-1a) ASF suppressed A (H-2a, Ig-1e) but not C3H.A (H-2a, Ig-1a) or DBA/2 (H-2d, Ig-1c). Separate ASF molecules may react with separate antigens on the cell surface, i.e., with H-2 and gammaG2a. Alternatively, one ASF molecule may react with two structurally associated antigens. If the latter is correct, it is conceivable that the beta2-microglobulin which is non-covalently linked to the major component of H-2 molecules expresses allotypic antigens coded for by Ig-1 and beta2-microglobulin is one of the antigens recognized by ASF.
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PMID:Suppression of antibody responses in allogeneic mice by products of lymphoid tissue. II. Lack of antigenic specificity and immunogenetic requirements of allogeneic suppressive factor (ASF). 5 47

Spleen cells harvested from mixed leukocyte cultures (MLC) on day 2 or 3 suppress the development of CL from a fresh MLC across a cell-impermeable membrane, but day 4 MLC cells which have the maximum level of CL showed only a limited effect. Inhibition was observed only when suppressor cells were restimulated with the same H-2 type cells used during induction. However, the suppressive effect was not strain specific; that is, CBA-induced C57BL/6 spleen cells effectively inhibited the development of CL from DBA/2-induced C57BL/6 cells. In addition, DBA/2-induced C57BL/6 spleen cells effectively inhibited the development of CL from CBA cells. B10 spleen cells stimulated by B10.D2 cells gave rise to a suppressor cell population, indicating that H-2 differences alone can induce the response. The suppressive effect seemed to be exerted on an early phase of the response since no detectable inhibition was observed when suppressor cells were added 48 hr after culture initiation. The suppressive effect is not exerted on the accessory cell function but seems to inhibit DNA synthesis of the reacting cells in the MLC.
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PMID:Cell-mediated immune response in vitro. II. The mechanism(s) involved in the suppression of the development of cytotoxic lymphocytes. 6 10

Spleen cells from mice homozygous for the obese (ob) mutation killed DBA/2 mastocytoma target cells less well than spleen cells from lean littermates or unrelated age-and sex-matched controls of the same strain. Killing was impaired only when the attacker cells were primed in vivo, not following in vitro priming. Hence the effect of the ob/ob genotype is not to produce an irreversible functional change in the lymphocyte, but rather to produce an environment in which lymphocytes are less able to react to priming antigen. Not only were the spleen cells of in vivo primed obese mice less active than those of lean controls, but also their number per spleen was significantly decreased. Such a quantitive difference was no longer found in adrenalectomised animals, but the qualitative difference in spleen cell cytotoxic activity still occurred. This suggests that adrenocortical hyperfunction may affect immune function in obese mice, without necessarily being the only factor in the in vivo environment of obese mouse spleen cells capable of depressing cellular immune reactivity.
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PMID:Effects of the obese (ob/ob) genotype on spleen cell immune function. 10 17

The ovarian-hormone-induced leukaemias of strain ICRC mice, with an abundance of intracytoplasmic type A particles in primary as well as transplanted lesions, were used to study morphological, biophysical, immunological and structural characteristics of type A particles. Mammary tumours of strains ICRC and C3H(Jax) were also used as sources for type A particles. The purified virions banded at the density of 1.20 g/ml in 12--60% linear sucrose-density gradient when subjected to spinning at 113,000 g for 4 h. The SDS-polyacrylamide-gel electrophoresis of type A particles from mammary tumours and leukaemias reproducibly resolved at least 8 polypeptides, 2 of these 54,000 and 24,000 dalton proteins, showing variable expression. Type A particles and B particles, despite the fact that each had a distinct polypeptide pattern, showed common antigens with different electrophoretic mobilities. Proteins of 24,000, 18,000 and 12,000 daltons from B particles were found to be antigenically related to those from type A particles. The bioassay studies carried out with purified A particles showed that 2/7 males of strain ICRC and 1/6 females of strain DBA-MTI developed leukaemias, as against none in the controls, when inoculated between the ages of 1-7 days. Spleen tumour and cervical tumour were seen in one female each of strain DBA-MTI.
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PMID:Intracytoplasmic type A particles from mammary tumours and leukaemias of strain ICRC mice. 10 57

Spleen cells from mice with syngeneic tumor transplants are hyporesponsive in mixed-lymphocyte culture. The hyporesponsiveness is due to the activation of suppressor cells. Spleen from tumor-bearing mice, treated with mitomycin and added to normal mixed lymphocyte culture (with responding cells syngeneic to the added cells), inhibits proliferation of the responding cells. Suppressor activity in the spleen cells can be detected as early as 5 days after s.c. transplantation of P-815 mastocytoma into DBA/2 mice. Tumor cells placed in cell-impermeable i.p. diffusion chambers can also activate splenic suppressor cells. Suppressor cells can be activated in syngeneic mice by (DBA/2) P-815 cells, by (C3H) L25-cells, or by recent (C57BL/6) methylcholanthrene-induced tumors. The latter tumors retain their ability to activate suppressor cells after passaging in syngeneic mice. Only one tumor, induced with methylcholanthrene in DBA/2 mice, failed to activate suppressor cells. Suppressor activity in the spleen cells from mice with 20-day s.c. tumor transplants is not reduced after removal of glass-adherent cells. Suppressor activity is significantly decreased after removal of thymus-derived cells with anti-theta treatment and complement.
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PMID:Activation of suppressor cells by syngeneic tumor transplants in mice. 14 32


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