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)

In these studies, we have compared the effects of anti-mu and anti-delta antibodies on normal and neoplastic murine B cells. Spleen cells from normal BALB/c mice or from mice carrying the BCL1 tumor were treated with F(ab')2 fragments of affinity purified anti-mu or anti-delta antibodies and the effec of the antibodies on cell proliferation was assessed. F(ab)'2 fragments of both antibodies induced proliferation of normal adult B cells but inhibited (anti-mu) or had no effect (anti-delta) on proliferation of BCL1 cells. In addition, both antibodies further enhanced the LPS-induced proliferative response of cells from adult mice. In contrast, the LPS responses of neonatal cells and BCL1 cells were inhibited by F(ab')2 anti-mu antibodies. These data indicate that interaction of antibody with surface IgD as well as surface IgM can activate adult B cells. In addition, the results provide further evidence that BCL1 cells are neoplastic analogs of immature B cells since the tumor cells, like neonatal cells, are not activated after treatment with anti-Ig antibodies.
 ...
PMID:The effect of anti-immunoglobulin antibodies on the in vitro proliferation and differentiation of normal and neoplastic murineB cells. 677 32

Spleen cells of two rat strains, Lewis and Brown Norway (BN), have been activated by lectins and by antibodies specific for immunoglobulin isotypes embedded in their cell membranes. Optimal concentrations of antibodies specific for mu, gamma, or delta-chains of rat augments in vitro incorporation of 3H-TdR 5 to 18-fold in Lewis B lymphocytes and 1.5 to 4-fold in BN B lymphocytes. In addition, F(ab')2 fragments of anti-Ig reagents induced Lewis splenic B cells but not BN B cells to incorporate 3H-TdR. Responses to LPS and dextran sulfate, B lymphocyte mitogens, measured by radioactive uptake, were five to 10 times greater in Lewis B cell populations than in BN B cell populations. Density of surface Ig isotypes and capping kinetics were similar in the two rat strains, although the percentage of T cells, T cell subsets, B cells, and Ia+ B cells differed in the spleens of these strains of rats. Both T lymphocytes and macrophages were needed in culture to effect an optimal response. IL-2 restored the response in B cell cultures depleted of T cells and macrophages, and enhanced 3H-TdR uptake in whole spleen cells of Lewis but not BN rats. The strain-dependent responsiveness of B cells to specific anti-Ig reagents or B cell mitogens appears to be associated with inherent (genetic) defects in T cells and B cells or defects in T cell to B cell cooperation in BN rats.
 ...
PMID:Activation of rat B lymphocytes. I. Characterization of anti-immunoglobulin responses and isotype density of rat B cells. 679 18

Concentrations of diethylstilbestrol phosphate (DES-P) and estramustine phosphate (EMP) above 10(-5) M in cultures of spleen lymphocytes from adult male mice resulted in a dose related inhibition of both Con A and LPS induced lymphocyte proliferation. Male mice injected with 5.6 mg./kg. DES daily for 7 days had a significantly reduced responsiveness to both Con A and LPS compared to mice injected with olive oil only. Spleen lymphocytes from male mice treated with 100 mg./kg. EMP showed a reduction of Con A induced mitogenesis whereas they exhibited a significantly enhanced response to LPS. The effects of DES and EMP on Con A and LPS induced blastogenesis were abolished within 2 weeks after cessation of treatment. DES treatment resulted in preferential depletion of splenic and lymph node T lymphocytes and a disproportionate T lymphocyte subpopulation with respect to Ly subclasses. Exposure to 30 or 100 mg./kg. EMP resulted in a dose related loss of mononuclear cells both in spleen and lymph nodes. T lymphocytes predominantly of the Ly 1 phenotype were most sensitive to EMP. Co-cultures of spleen lymphocytes from normal mice and Mitomycin C blocked spleen cells from either normal of treated mice (DES or EMP) gave no convincing evidence of suppressor cell activity in the population of spleen mononuclear cells.
 ...
PMID:Effects of diethylstilbestrol and estramustine phosphate (Estracyt) on lymphoid cell populations and mitogen responsiveness in male mice. 698 78

Spleen cells from mice sensitized with 10 microgram of LPS given intravenously are unable, when stimulated in vitro 48 h after this treatment, to respond to sheep erythrocytes (SRBC). Addition of T-cell replacing factors (TRF) to these cells restores their capacity to mount an anti-SRBC immune response. Killing of the cells proliferating under antigen stimulation by highly radioactive thymidine leads to the suppression of the anti-SRBC response observed in the presence of TRF. These experiments suggests that the proliferative events leading to the expansion of B cell precursors under antigen stimulation is not impaired by the treatment by LPS. These preliminary data show that the defect is linked to the lack of signals leading to the differentiation of B cells into antibody-secreting cells.
 ...
PMID:Differentiation signal defect of splenic cells from LPS-treated mice. 700 15

As has been found for spleen cells from ageing NZB x NZW (B/W) mice, ageing NZB mice were also found to make no antibody when stimulated in vitro with the polyclonal B cell activators (PBA) LPS and PPD. This immune defect was not due to the action of suppressor cells, since old NZB and B/W spleen cells did not suppress the PBA response of young spleen cells. Spleen cells from aged NZB mice were not able to generate antibody-forming cells when stimulated with the thymus-independent antigen, TNP-LPS, but were able to produce antibody in response to another thymus-independent antigen, TNP-AECM-Ficoll, thereby implying that there is a selective functional deletion of a B cell subpopulation in ageing New Zealand mice. The failure of B/W and NZB spleen cells to generate antibody in response to PBA is interpreted as a consequence of a continuing in vivo polyclonal B cell activation accompanying the development of autoimmune disease, leading to a scarcity of B cells available for activation by PBA and by some thymus-independent antigens in vitro.
 ...
PMID:Functional absence of a B cell subpopulation in ageing New Zealand mice. 700 89

Lymphoid cell populations (spleen, lymph node, peripheral blood, thymus, and bone marrow) from LHC inbred hamsters were studied in order to characterize further the immune response of this species. The direct PFC response to several thymic-dependent or thymic-independent antigens was evaluated. A specific direct PFC response occurred 4 days after immunization with SRBC, DNP-BSA, DNP-lys-Ficoll, TNP-LPS, TNP-BA, and SSS-III. Attempts to induce a polyclonal antibody response with LPS, TNP-LPS, SSS-III, and DNP-lys-Ficoll were unsuccessful. A weak polyclonal response was induced with TNP-BA. Spleen cells and PBL responded strongly in vitro to the T-cell mitogens Con A and PHA-P, but gave weak and inconsistent responses to the B-cell mitogens LPS and PI-PC. LHC hamster lymphoid cell populations bore sIg and receptors for C3 (EAC rosettes) in approximately the same ratio as various murine species. However, the profile of the number of cells bearing low-to-intermediate densities of sIg differed significantly from those of murine species when analysed with the FACS. There was a sharp reduction in the number of cells with low-to-intermediate densities of sIg. These data suggest that B cells in this strain and species lack the ability to translate signals which lead to polyclonal antibody synthesis or lack the appropriate populations of B cells that have membrane receptors for mitogens which are thought to induce such activity in murine systems and provide evidence for separate signals that induce thymus-independent and mitogenic responses. The importance of this model for studying mechanisms involved in B-cell activation is discussed.
 ...
PMID:In vitro and in vivo response of lymphoid cells from LHC hamsters to murine thymus-independent and thymus-dependent antigens. 700 14

Spleen and mesenteric lymph node cell blastogenic responses to the mitogens concanavalin A and lipopolysaccharide and to parasite antigens were examined in vitro following removal from mice undergoing primary or secondary infection with Nippostrongylus brasiliensis. During primary infection spleen cells showed a marked increase in proliferative responsiveness to both mitogens, followed by a marked depression thereafter. During a secondary infection the response of spleen cells to both mitogens remained depressed. In contrast, cells from the mesenteric lymph nodes of infected mice exhibited enhanced responsiveness to Con A and LPS, followed by depression of the response, followed by another cycle of enhancement upon reinfection. Sensitivity of both spleen and especially mesenteric lymph node cells to Nb antigens was greatest at approximately the time of worm expulsion: Day 13 after primary and Day 8 after secondary infection.
 ...
PMID:Modulation of lymphoid cell blastogenic responsiveness to mitogens by Nippostrongylus brasiliensis infection. 703 66

In BALB/c mice, the injection of pristane resulted in a severe decrease in splenic T and B cell proliferative responses to mitogens and in a depression of natural killer (NK) activity. The effects of T and B cells, which persisted for at least 5 mo, were mediated by different mechanisms. T cell responsiveness to PHA dropped significantly below control levels 1 wk after the first of three monthly pristane injections, whereas B cell proliferation in response to LPS did not decrease until 4 wk after the first injection. The removal of plastic-adherent suppressor cells completely restored T cell proliferative capacity, but had no effect on B cells. NK activity against YAC-1 tumor targets was reduced 1 mo after the first pristane injection and remained depressed for at least 3 mo. This depression was not mediated by plastic-adherent suppressor cells. Spleen cell NK activity from pristane-treated mice could not be augmented by the interferon inducer Poly I:C to the same extent as that of control mice. This suggests an effect of pristane on either pre-NK cells or on cells that regulate NK activity.
 ...
PMID:Depression of natural killer activity and mitogen responsiveness in mice treated with pristane. 714 8

Disturbances in suppressor cell function have been considered important in the pathogenesis of systemic lupus erythematosus (SLE), a conclusion supported by studies with New Zealand mice. To determine whether other SLE mice display similar immunoregulatory defects, we investigated the susceptibility of autoimmune MRL mice to unresponsiveness induced by hapten-modified self (HMS). The response of splenocytes from MRL-lpr/lpr mice (lpr) was compared with those of sex- and age-matched, congenic MRL-+/+ mice (+/+), and H-2-identical (H-2k) CBA/J mice. Spleen cells (NSC) were cultured in vitro with hapten-modified syngeneic splenocytes (TNP-SC) and tested for responsiveness to TNP-LPS (for tolerance) or their ability to suppress the response of fresh cells. There was no difference in the susceptibility of lpr splenocytes from 3- and 10-mo-old mice to the induction of tolerance or suppression when compared with those from age-matched +/+ or CBA mice. To evaluate any quantitative defects in the responsiveness of lpr splenocytes to HMS, we modified the conditions under which suppressor activity was generated. Varying the ratio of NSC to TNP-SC from 10:1 to 2000:1, or changing the concentration of TNBS for haptenation from 10 mM to 0.5 mM per 10(8) spleen cells revealed no differences in the dose-response curves of lpr splenocytes for both tolerance and suppression when compared with those of the CBA. These results indicate that clinically affected MRL mice have intact suppressor cell activity in response to antigen-modified self and suggest a possible therapeutic role of this modality in inducing tolerance to self-antigens.
 ...
PMID:The induction of tolerance and suppression in autoimmune MRL mice using hapten-modified self. 725 56

In vitro mitogen-driven lymphocyte proliferation tests (Con A, LPS) on murine lymph node and spleen cells revealed inhibition of T and B cell stimulation by different benzodiazepines and by PK 11195, with IC50 values in the low micromolar range. T cell responses as a consequence of recognition of alloantigens, as measured in mixed lymphocyte cultures (MLC), were affected in an analogous way. In all systems, agonists at peripheral type benzodiazepine receptors (Ro 5-4864 and the non-benzodiazepine compound PK 11195) and diazepam which acts on both, central and peripheral type benzodiazepine receptors, were most potent; clonazepam, a central type agonist, proved about half as active. The central type antagonist Ro 15-1788 failed to antagonize the action of diazepam and clonazepam. Variations among cells from several congenic strains of mice were modest. Cytotoxicity could not be made responsible for drug effects. The most susceptible stage of mitogen-triggered T and B lymphocyte proliferation was found to be at incipience. Radioresistant, adherent spleen cells, upon LPS-stimulation formed only small amounts of the cytokine IL-1. Its release was affected only at very high drug concentrations. Similar small amounts of IL-1 were generated during MLC; in this case, the drugs were about 10 times less potent than in mitogen-induced proliferation assays. Peripheral agonists were more active on IL-1 synthesis. Spleen cells stimulated with Con A and cultivated with the highest concentration of diazepam and clonazepam formed markedly greater amounts of IL-2 than those cultivated in medium, while at this concentration PK 11195 allowed no formation of the lymphokine.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:In vitro inhibition of cellular immune responses by benzodiazepines and PK 11195. Effects on mitogen- and alloantigen-driven lymphocyte proliferation and on IL-1, IL-2 synthesis and IL-2 receptor expression. 830 Oct 19


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>