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)

Cyclosporine treatment of BALB/c mice (at a dose of 20 mg/kg every other day for 3 weeks) caused a remarkable reduction in the PNA-, L3T4+Lyt-2- subset of thymocytes. A significant reduction of the L3T4+Lyt-2-subset was also observed in both the lymph node and spleen cells of CsA-treated mice, though the degree of the reduction was lower than that in thymocytes. Both lymph node and spleen cells from CsA-treated mice showed a significant increase in the percentage of Thy-1.2 negative, L3T4-Lyt-2- cells (perhaps B cells). Thymocytes from CsA-treated mice showed a reduction in the in vitro proliferative responses to Con A and PHA. On the other hand, there was a slight, but not significant, decrease in the responses of lymph node cells to Con A, PHA and LPS. Spleen cells from CsA-treated mice showed a significant reduction in the responses to Con A and PHA, though the degree of the reduction was lower than that of thymocytes. There was a significant decrease in the proliferative response of spleen cells to LPS. These results suggest that CsA affects both thymus and spleen cells in vivo, preferentially impairing the L3T4+Lyt-2- subset (helper T cells or their precursors) within the thymus. The lymph node cells seem to be relatively spared from the in vivo effect of CsA compared with cells in the thymus and spleen.
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PMID:Differential effect of cyclosporine in vivo on the distribution of T cell subsets in the thymus, spleen, and lymph nodes. 278 40

It is widely recognized that various microorganisms including viruses have immunomodulatory effects and, under appropriate circumstances, may markedly suppress the immune response mechanisms. Cannabinoids present in marijuana also have immunomodulatory effects. In the present studies THC as well as its metabolic product 11-OH THC were studied in regard to their effects in vivo and in vitro on selected parameters of the immune response system known to be important in antiviral resistance, including immunity to retroviruses. Cannabinoids markedly suppressed the ability of murine macrophages to spread on glass (an important functional marker of macrophages) as well as to phagocytize yeast particles. Splenic macrophage cultures treated with the cannabinoids also were deficient in their ability to produce interleukin 1 on appropriate stimulation with bacterial LPS. Spleen cells capable of producing antibody to sheep erythrocytes when stimulated with this antigen in vitro were markedly affected when treated with graded doses of THC or 11-OH THC. Furthermore, the blastogenic responsiveness of normal mouse splenocytes to the T-cell mitogens Con A and PHA as well as the B-cell mitogen E. coli LPS was markedly suppressed by graded concentrations of the cannabinoids in doses that did not affect the viability of the cells. Natural killer cell activity of normal mouse spleen cells was also markedly inhibited by THC and 11-OH THC. Similarly, these cannabinoids suppressed the blastogenic responsiveness and NK activity of human peripheral blood leukocytes from normal individuals. The ability of mouse spleen cells to produce interferon on in vitro stimulation was also suppressed by THC. In addition, injection of THC into mice suppressed blastogenic responsiveness of spleen cells, NK activity, and the production of interferon by lymphoid cells. Thus, it was apparent that these cannabinoids had immunomodulatory effects, both in vivo and in vitro, at noncytotoxic small doses and impaired the ability of the lymphoid cells to express immune function necessary for antiviral resistance.
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PMID:Drugs of abuse and virus susceptibility. 284 Aug 2

Spleen cell blastogenesis to mitogens and antibody responses to sheep erythrocytes (sRBC) were tested in BALB/c mice with experimental E. cuniculi infections. Blastogenesis responses of spleen cells 1 week post-infection were significantly lower than normal to T-cell mitogens (Con A and PHA) and were unchanged in response to B-cell mitogens (LPS and PWM). After 2 weeks post-infection, the responses to T cell mitogens returned to normal. Mixing spleen cells from 1-week infected mice with cells from uninfected mice failed to reveal the presence of suppressor cells. Antibody responses to sRBC were significantly slower to develop in 1 week-infected mice compared with uninfected mice or mice infected 2 weeks earlier or at the same time as sRBC challenge. Infected mice displayed splenomegaly which was most pronounced 1 week post-infection and the differential spleen cell counts revealed the presence of lymphoblasts. Lymphohyperplasia appeared to cause the splenomegaly. No shifts in the proportion of Thy 1.2+ T cells, Ig+ B cells, or esterase-positive macrophages were detected. These results indicate that the immune system in BALB/c mice is depressed early during E. cuniculi infections.
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PMID:Modulated immune responsiveness associated with experimental Encephalitozoon cuniculi infection in BALB/c mice. 297 36

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

Primary cultures of adult rat hepatocytes (Fischer 344) were used as an in vitro metabolic activation system in immunotoxicological assays. Rat hepatocytes were isolated by a collagenase perfusion technique and cultured for 20 to 24 hr to allow the formation of a monolayer on collagen-coated plastic petri dishes. Spleen cells isolated from (C57BL/6 X C3H)F1 mice were cocultured with the hepatocytes along with the chemicals. Cyclophosphamide (CP) and Aflatoxin B1 (AFB1) were effectively activated in this coculture system and produced a dose-related suppression of the in vitro antibody responses to LPS, DNP-Ficoll, and SRBC in 3 hr. Neither CP (1 mM) nor AFB1 (10(-4) M) cultured with spleen cells alone produced any effects. Both CP and AFB1 also produced a dose-related suppression of the proliferative responses to LPS, Con A, and PHA. In contrast, up to 100 mM of N-nitrosodimethylamine (DMN) did not suppress any of these assays after a 3-hr incubation in the coculture system. These results indicate that a coculture system can be used to characterize the activity of immunosuppressive chemicals requiring metabolic activation.
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PMID:Immunosuppression induced by chemicals requiring metabolic activation in mixed cultures of rat hepatocytes and murine splenocytes. 308 86

Histamine is known to mediate potent immunosuppressive effects on lymphocyte function. In jirds infected with Brugia pahangi decreased mitogen and parasite antigen responsiveness are associated with the presence of histamine binding regulatory cells. The present study was thus designed to investigate the immunoregulatory role of histamine in experimental filariasis. Spleen cells from normal or B. pahangi infected jirds were incubated with BSA or histamine coupled Sepharose beads and the degree of cell-bead binding was quantitated. Cells from infected jirds demonstrated increased levels of histamine, but not BSA binding relative to normal cells, and this binding was blocked by soluble histamine or by the histamine receptor antagonist cimetidine. Cimetidine failed to restore the in vitro responsiveness of spleen cells from infected jirds to phytohemagglutinin or to a soluble extract of B. pahangi. Cimetidine did, however, reverse histamine-induced suppression of normal spleen cell responses to PHA. The present results suggest that histamine does not play a major role in the immunoregulatory alterations induced by B. pahangi infection.
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PMID:Failure of the H2 antagonist cimetidine to reverse parasite antigen-specific lymphocyte unresponsiveness in experimental filariasis. 321 1

Bone marrow and spleen cells obtained from female B6C3F1 mice given a single i.p. exposure to cadmium acetate (0.9 mg/kg), lead acetate (12 mg/kg), or sodium acetate (12 mg/kg), were studied using flow cytometry, immunologic, and hematologic assays. Significant changes were detected in subpopulations of bone marrow cells using multiparameter flow cytometry within 1 day following treatment with cadmium or lead. Bone marrow cells obtained from B6C3F1 mice 5 days after treatment with cadmium or lead were found to have a decreased number of cells expressing Mac-1, 55-7.2, 14.8, and Lyt-1 antigens, suggesting a shift to immature cell types. An increase in the number of progenitor cells (CFU-C) obtained from the bone marrow of mice treated with heavy metals was also noted 5 days after exposure to cadmium or lead. A time-dependent suppression of the in vitro primary humoral immune response of spleen cells to SRBCs, TNP-Ficoll and TNP-LPS was produced by cadmium or lead treatment. Suppression of the mitogenic response of spleen cells to Con A, PHA, and LPS was also found to be time-dependent. Spleen cell surface marker expression (Mac-1, Lyt-1, Lyt-2 and 14.8) was altered in response to cadmium or lead treatments, but these changes did not appear to correlate with the humoral immunity or mitogen-induced proliferation data. These studies demonstrate that changes in cell surface markers on discrete subpopulations of lymphoid cells present in the spleens of heavy metal exposed mice may not correlate with alterations in the functional activity of these cells. However, changes in murine bone marrow surface markers in response to cadmium or lead treatment predicts a shift to immature cell types, which appeared to correlate with the increase in CFU-C activity.
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PMID:Analysis of heavy metal immunotoxicity by multiparameter flow cytometry: correlation of flow cytometry and immune function data in B6CF1 mice. 362 73

The colony-stimulating factor CSF-2 alpha (IL 3) has been purified to homogeneity, the protein sequenced, and the gene encoding this lymphokine cloned. Knowledge of the protein sequence permitted the synthesis of peptides corresponding to the amino terminus of the molecule. These peptides, after conjugation to palmitic acid, were used to immunize mice. Spleen cells from mice immunized with one of these peptides (CSF-2 alpha 1-14) were fused with the myeloma cell line NS-1. The fusion resulted in the isolation of two hybridoma cell lines, designated 6A5 and 4D4, that secreted antibodies that were specific for the immunizing peptide. The antibodies did not react with a closely related peptide CSF-2 alpha 7-16. The antibodies were capable, however, of recognized CSF-2 alpha protein as judged by the ability of the antibodies to remove CSF-2 alpha activity from culture medium of PHA-stimulated LBRM-33-5A4 cells, to immunoprecipitate radiolabeled CSF-2 alpha protein, and to detect CSF-2 alpha protein bound to nitrocellulose membranes.
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PMID:Generation of anti-peptide monoclonal antibodies which recognize mature CSF-2 alpha (IL 3) protein. 392 4

Cultures of chicken lymphoid tissues were tested for their capacity to lyse (51)Cr-labeled chicken, burro (BRC), and human red blood cells (HRC) in the presence of phytomitogens. PHA-stimulated cultures lysed all three types of targets, while PWM and Con A showed a "target cell specificity" for HRC and BRC, respectively. In mixtures of target cells only the appropriate targets were lysed by lymphocytes activated by either Con A or PWM indicating that soluble lymphotoxins do not play a major role in these reactions. Preincubation experiments suggested that there may be a population of pre-existing aggressor cells which only require linking to the targets by the mitogens for activation of their cytotoxic potential. Strong cytotoxic reactions were found with spleen cells, peripheral blood leucocytes, and bone marrow cells. Thymocytes were less active but could be stimulated for significant cytotoxicity, while bursal cells were generally unreactive. Spleen cells from agammaglobulinemic chickens totally lacking serum immunoglobulins and B cells with surface-bound immunoglobulins were as active as cells from normal chickens. The activity of spleen cells, from which phagocytic cells were removed was also unimpaired. These results indicate that the development of cytotoxic effector lymphocytes in mitogen-treated leucocyte cultures is a property of T lymphocytes. Although bone marrow cells fail to proliferate in response to these phytomitogens, they do have strong cytotoxic reactivity suggesting that different subsets of thymic-derived lymphocytes are responsible for mitogen-induced transformation and mitogen-induced cytotoxicity.
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PMID:Pokeweed mitogen-, concanavalin A-, and phytohemagglutinin-induced development of cytotoxic effector lymphocytes. An evaluation of the mechanisms of T cell-mediated cytotoxicity. 454 36

A microcytotoxicity assay to prove directly against myelin basic protein directed cytotoxic T cells has been developed. Spleen and lymph node cells of myelin basic protein immunized strain 13 guinea pigs were restimulated in vitro with basic protein for 5 days and used as attacking cells. Autologous spleen cells were coated with about 10(7) molecules basic protein by hydrophobic attachment, labelled with 51Cr and used as targets. Concentration dependent lysis (74% corrected lysis) was measured with attackers gained 12 days post immunization. Controls performed using unspecific (PHA) stimulated attackers and non BE coated target showed no lysis. Lysis was shown to be MHC restricted. The test may serve as a tool for the assay of human demyelinating diseases.
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PMID:Direct proof of autoreactive T-lymphocytes in experimental allergical encephalomyelitis (EAE). 616 38


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