Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P43026 (lipopolysaccharide)
 62,215 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

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 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

Cell-mediated and humoral immune responses were assessed in mice at mid-term (day 10) in pregnancy. A significant but selective suppression of the primary in vivo antibody (plaque-forming cell) response to SRBC was observed, with the most pronounced effect being on the gammaA response. Similar results were obtained for secondary in vitro antibody synthesis by antigen-primed spleen cells from pregnant mice, demonstrating the intrinsic nature of the inhibition. Pregnant mouse serum (PMS) was shown to suppress primary in vitro antibody synthesis, and the inhibitory effect was abrogated by the selective removal of alpha-fetoprotein (AFP) using affinity chromatography. Normal mouse serum became similarly suppressive in vitro when purified AFP of fetal origin was added to it in concentrations approximating that found in PMS. Spleen cells from pregnant mice showed a suppressed mitogenic response to phytohemagglutinin, a lowered response to concanavalin. A, and a normal response to lipopolysaccharide. In contrast, the allogeneic response of these animals as measured in the one-way mixed lymphocyte culture was enhanced. PMS suppressed both allogeneic and mitogen-induced lymphocyte transformation by spleen cells from nonpregnant mice, and the effect was eliminated by the selective removal of AFP. These findings indicate an important functional role for AFP in normal embryological development.
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PMID:The immunosuppressive role of alpha-fetoprotein during pregnancy. 6 86

Infection with Trypanosoma cruzi decreases the ability of spleen cells from mice to respond to either T cell, concanavalin A (Con A), or B cell, lipopolysaccharide (LPS), mitogens. The effect of infection on the mitogenic response depends on the elapsed time between the day of infection and the time of mitogen presentation. Responses early in infection are normal, whereas later responses to either mitogen are depressed. Spleen cells from late trypanosome-infected mice inhibit the ability of normal spleen cells to respond to Con A or LPS. The cell in the T. cruzi-infected spleen cells responsible for this effect is nonadherent, sensitive to treatment with anti-mouse thymus serum plus complement, but insensitive to treatment with anti-immunoglobulin plus complement. These data indicate that infection with T. cruzi elicits over time the generation of T cells suppressive to T and B cell mitogenic responses.
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PMID:Suppressor cells present in the spleens of Trypanosoma cruzi-infected mice. 10 8

Spleen cells from trypanosome-infected mice strongly suppressed lymphocyte stimulation induced in normal spleen cell populations by lipopolysaccharide, concanavalin A or allogeneic (H-2-different) stimulator cells. This suppression was not H-2-restricted, as responses of spleen lymphocytes both allogeneic and syngeneic to the suppressors were inhibited. Irradiation or mitomycin C treatment of suppressor populations markedly reduced but did not eliminate suppressor activity. Suppressor populations were effective when present in very low numbers. Addition of suppressor cells to mixed lymphocyte cultures at various intervals after initiation of the cultures showed that the suppressors require 48 h to manifest their activity. Cell depletion or enrichment experiments indicate that the mechanism of suppression is complex and involves more than one cell type.
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PMID:Immune depression in trypanosome-infected mice. III. suppressor cells. 15 20

Old (15-20 month) male (NZB x NZW)F1 (B/W) mice have severely impaired spleen cell reactivity to phytohemagglutinin (PHA), a mitogen which stimulates mainly T lymphocytes. Spleen cells from old mice markedly suppressed the PHA response of splenocytes from young (3-4 month) B/W males. Similar suppressor activity was not present in the spleens of old mice of four nonautoimmune strains. The suppressor activity of old B/W spleen cells was mediated by a nonphagocytic, radioresistant, mononuclear leukocyte. Although this cell was eluted in the "T lymphocyte" fraction of nylon wool colums, it was not sensitive to treatment with anti-Thy-1 antiserum and complement. Suppressor activity was lost after 18 h incubation at 37 degrees C in tissue culture medium. Supernatants of these overnight cultures had no suppressive effect on fresh young B/W spleen cells. Old B/W spleen cells suppressed PHA reactivity more than concanavalin A or lipopolysaccharide reactivity. Kinetic studies demonstrated an increasing suppression with time over 72 h of culture. This study demonstrate that the severely impaired PHA reactivity of old B/W mice is mediated, at least in part, by active suppression.
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PMID:Suppressor cells and immunodeficiency in (NZB x NZW)F1 hybrid mice. 15 83

BALB/c spleen cells (5 x 10(6)) were cultured in 1 ml of serum-free RPMI 1640 medium for 3 days in order to examine the effect of cholera enterotoxin (CN) and its spontaneously formed toxoid (CD) on lymphocyte stimulation. Stimulation was assessed after addition of [3H] thymidine for the last 16 hours of culture. One microgram of CN per culture markedly reduced the baseline of [3H] thymidine incorporation and the stimulation due to phytohaemagglutinin (PHA), concanavalin A (con A) and bacterial lipopolysaccharide (LPS). One microgram of CD diminished the base-line to half, abolished the response to PHA, reduced the response to con A and had very little effect on the LPS-induced stimulation. One-tenth the amount (0-1 mug) of both CN and CD affected only the PHA reaction. A secondary response to haemocyanin in vitro was not decreased by this lower dose. The effect of 1 mug on CN on the LPS response could be reduced by pretreatment of the cells with CD, whereas the PHA reaction remained markedly diminished. Dibutyryl-cAMP added to culture tubes had a similar effect ot 1 mug of CN, affecting the PHA response much more than the response to LPS. Spleen cells of mice immunized with CD gave a significant proliferative response to both 1 mug of CD and CN. The results are interpreted as indicating a strong inhibitory effect of CN mediated by accumulation of intracellular cAMP. CD-immunized cells contain specific receptors for both CD and CN which probably compete with the sites responsible for adenylate cyclase stimulation by CN.
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PMID:The differential effect of cholera toxin on the lymphocyte stimulation induced by various mitogens. 16 98

Murine lymphoid cells were infected in vitro with WN 1802 B, a naturally occurring murine leukemia virus isolated from the spleen of an 18-month-old BALB/c mouse. Normal spleen and bone marrow cells were more susceptible to infection than were cells prepared from thymus and lymph node. Spleen cells from athymic nu/nu mice also could be readily infected with virus. Permissive cells did not ingest iron readily infected with virus. Permissive cells did not ingest iron filings and did not adhere to plastic. Exogenous replication of murine leukemia virus was enhanced in spleen and lymph node cells treated with lipopolysaccharide, a bone marrow-derived lymphocyte mitogen. Conversely, cells treated with the thymus-derived lymphocyte cell mitogens, phytohemagglutinin and concanavalin A, were less capable of supporting murine leukemia virus replication. These studies suggest that the natural host for WN 1802 B is the bone marrow-derived lymphocyte.
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PMID:Replication of murine leukemia virus in bone marrow-derived lymphocytes. 18 25

Spleen cells removed from C57Bl/6J mice bearing a methylcholanthrene-induced fibrosarcoma (MC-16) demonstrate suppressed responsiveness of phytohemagglutinin (PHA) and bacterial lipopolysaccharide (LPS) induced mitogenesis as compared to non-tumorous mice. A similar depression of PHA-induced mitogenesis was observed with spleen cells from C3H/HeJ mice bearing syngeneic mammary adenocarcinomas (C3HBA). The administration of indomethacin, a non-competitive irreversible prostaglandin (Pg) synthesis inhibitor, (75 or 100 mug/mouse, IP) on an alternate day basis to groups of tumor-bearing mice of both strains, significantly enhanced immune cell responsiveness to mitogenic stimulation. The addition of indomethacin (10 mug/ml) to cultures of spleen cells from these tumor-bearing mice, as well as to DBA/1J mice bearing the Cloudman S-91 melanoma, enhanced spleen-cell responsiveness to mitogen-induced DNA synthesis by as much as 156%. Indomethacin administration in vivo or in vitro had no significant effect on mitogen-induced DNA synthesis of spleen cells from non-tumor-bearing animals. It is hypothesized that tumors, or tumor-cell antigens, increase Pg production of a population of spleen cells, and that the increased Pg content of the spleen may be important in controlling immune responsiveness in mice.
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PMID:Indomethacin enhancement of spleen-cell responsiveness to mitogen stimulation in tumorous mice. 18 13


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