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)

This study describes the development of IgM and IgG containing plasmablasts in splenic white pulp after a single intravenous injection of the thymus-independent antigen lipopolysaccharide (LPS) or the thymus-dependent antigen sheep erythrocytes (SRBC) using immunohistoperoxidase techniques. Attention has been paid especially to the sites where IgM and IgG blasts develop in the white pulp and their migration route, from the white pulp towards the red pulp. The distribution of IgM and IgG blasts in the different white pulp compartments, i.e. outer periarteriolar lymphocytic sheath (PALS), inner PALS, follicles and the area along the terminal arteriolar branches, has been studied. Our findings indicate that both the thymus-independent IgM response to LPS and the thymus-dependent IgM response to SRBC start in the outer PALS. During the course of the immune response against SRBC the early localization of IgG plasmablasts in the white pulp was dispersed through the whole PALS. Later in the immune response the IgG blasts in the white pulp were localized especially in and at the border of follicle centres. No significant development of IgG blasts was found after LPS administration. The results of the present study suggest that during the immune response the bulk of IgM blasts migrates via the outer PALS and along the terminal arteriolar branches into the red pulp.
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PMID:The development of IgM- and IgG-containing plasmablasts in the white pulp of the spleen after stimulation with a thymus-independent antigen (LPS) and a thymus-dependent antigen (SRBC). 675 49

The biological and immunological characteristics of TC-13, an antitumor protein-bound polysaccharide, were studied. TC-13 had no direct cytocidal effect on Ehrlich carcinoma, but it induced antitumor resistance in mice whose tumors were regressed by TC-13. TC-13 changed the electrophoretic pattern of serum proteins of mice after its ip administration, causing a slow increase of the LB component and a rapid increase of the X component. TC-13 augmented the delayed-type hypersensitivity reaction to tumor homogenate, anti-SRBC antibody formation and the cytocidal activity of macrophages in an antibody-dependent system, but it had little or no effect on blast formation of spleen lymphocytes or carbon clearance. These results and comparative studies with other immunomodulators suggest that TC-13 is a unique polysaccharide having properties intermediate between those of lentinan, a simple-structured homologous polysaccharide from basidiomycetes, and lipopolysaccharide, a cell-surface component from bacteria.
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PMID:Comparative studies on immunological properties of antitumor polysaccharide TC-13. 675 88

The effect of thymus-derived lymphocytes (T cells) on the responsiveness of bone marrow-derived lymphocytes (B cells) to bacterial lipopolysaccharide (LPS) was determined in in vitro experiments. Radiation resistant splenic T cells obtained from euthymic nu/+ mice increased the number of proliferating cells in the cultures of splenic B cells from athymic nu/nu mice even in the nonstimulated state. The radiation resistant T cells augmented significantly the responsiveness of B cells to LPS, as determined by an increase in proliferating cells and polyclonally induced anti-sheep erythrocyte (SRBC) IgM hemolysin plaque-forming cells (PFC). Addition of the T cells to B cell cultures not only augmented the responsiveness of B cells to suboptimal doses of LPS but also enabled B cells to respond to supraoptimal doses of LPS. As is well documented, the radiation resistant T cells were unable to induce the generation of anti-SRBC PFC in B cell cultures, unless the cultures were simultaneously stimulated with SRBC. Colcemid, a specific inhibitor of cell mitosis, blocked almost completely the exponential generation of anti-SRBC PFC in B cell cultures responding to SRBC with the aid of radiation resistant T cells. In contrast, colcemid did not affect the exponential generation of anti-SRBC PFC of a polyclonal nature in B cell cultures responding to LPS, either in the presence or absence of radiation resistant T cells.
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PMID:Role of T cells in the mitogen-induced proliferation and polyclonal antibody response of murine B cells. 697 83

The first line of defense against pathogens that enter the host by the oral route appears to involve the gut-associated lymphoreticular tissue-e.g., Peyer's patches (PP). Although animals can readily be immunized by orally administered antigen that mobilizes the secretory immune system, there is a total lack of local antibody synthesis in the PP and the cellular basis for this deficiency remains a mystery. A lymphoreticular cell population, obtained when murine PP were treated with a neutral protease (Dispase), consisted of accessory cells [macrophages (MPhi)] and T and B lymphocytes. In vitro cultures of these PP cell preparations with the thymic-dependent antigen sheep erythrocytes (SRBC) resulted in good anti-SRBC plaque-forming cell (PFC) responses. The time courses of these responses were identical to those seen with spleen cell cultures. Submitogenic concentrations of concanavalin A (Con A) and optimal doses of N-acetylmuramyl-L-alanyl-D-isoglutamine (MDP) and lipopolysaccharide (LPS) enhanced in vitro responses of PP cell cultures to SRBC. PP possess fully functional antigen-presenting MPhi because incubation of optimal proportions of splenic T and B cells with purified populations of PP MPhi supported good in vitro immune responses. Murine PP possess all of the necessary elements for an IgA immune response because PP cell cultures derived from mice orally primed with SRBC and immunized with SRBC in vitro gave high IgA anti-SRBC PFC responses. All of the adjuvants tested (LPS, MDP, and Con A) enhanced IgA responses in PP cell cultures from orally primed mice; however, Con A induced the greatest enhancement. These results demonstrate that murine PP possess MPhi capable of accessory cell functions for in vitro immune responses and that oral priming with antigen induces the precursor T- and B-cell populations necessary for IgA responses, that are potentiated by adjuvants, in PP cell cultures. Thus, murine PP possess the lymphoreticular cells required for antibody responses; however, the tissue architecture likely prevents local responses in vivo. The finding that enzymatically dissociated PP contain all of the necessary cellular components for antibody synthesis, whereas the in vivo tissue architecture prevents the complex interactions necessary for this response, suggests that the initial inductive events take place in situ, and additional cell interactions are required for final differentiation of IgA-synthesizing plasma cells to occur at distant mucosal sites.
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PMID:In vivo immune response to a T-cell-dependent antigen by cultures of disassociated murine Peyer's patch. 697 42

Antibodies to the nuclear antigen SM are specific for systemic lupus erythematosus in humans and mice. In order to study the cellular mechanisms of anti-Sm generation, a hemolytic plaque assay to identify and enumerate lymphocytes secreting anti-Sm has been developed by using SRBC coated with purified Sm by a modified carbodiimide technique. Anti-Sm-specific PFC were found in MRL/Mp-Ipr/Ipr and MLR/Mp- +/+ mice whose sera contained anti-Sm, but were never detected in anti-Sm-negative MRL mice or in normals. Spleen cells from anti-Sm-positive MRL/Mp-Ipr/Ipr mice generated anti-Sm PFC spontaneously after 4 days of in vitro culture, whereas cells from normal mice or anti-Sm-negative MRL mice were never observed to produce spontaneous anti-Sm, even when cultured in the presence of bacterial lipopolysaccharide. The generation of anti-Sm by MRL cells in vitro was found to be dependent on the presence of T cells, but the ability of cells from individual MRL mice to generate anti-Sm appeared to be limited by the availability of Sm-specific B cell precursors and not due to a relative absence of T cells capable of providing help for the anti-Sm response. Analysis at the cellular level of the in vitro generation of a disease-specific autoantibody by using the methods described should facilitate understanding of mechanisms of autoreactivity.
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PMID:Anti-Sm autoantibodies in MRL mice: in vitro detection and generation of antibody-forming cells. 698 38

AKR mice were protected from lethal irradiation and established as long-lived chimeras by transplanting allogeneic C57BL/6 (B6) bone marrow that had been treated in vitro with anti-Thy-1 antiserum without complement. In these chimeras, which were designated [B6 {arrow} AKR], virtually all the thymus and spleen cells were shown to be derived from the B6 donor; several immune functions studied in these chimeras were as follows: (a) The chimeric mice were tolerant of histocompatibility antigens of both donor and recipient strain and nearly fully reactive to antigens of third party, as revealed by Simonsen's splenomegaly assay. The tolerance of these chimeras could not be attributed to suppressor cells but was compatible with clonal depletion. (b) Proliferative responses to concanavalin A, phytohemagglutinin, and lipopolysaccharide as well as natural killer and antibody-dependent cell- mediated cytotoxicity activity of the chimeric mice was normal. (c) Plaque- forming cell (PFC) assays of antibody responses to sheep erythrocytes (SRBC) showed gross deficiency in the primary response of the [B6 {arrow} AKR] and [AKR {arrow} B6] chimeras. By contrast, [B6-H-2(k)(E(k)) {arrow} AKR] H-2-compatible chimeras and [AKR {arrow} AKR] syngeneic marrow transplanted mice had normal primary PFC responses. PFC responses after secondary stimulation with SRBC, however, revealed vigorous direct plaque formation and substantial but somewhat smaller indirect plaque formation in the [B6 {arrow} AKR] chimeras. This observation favors operationally the concept of adaptive differentiation proposed by Katz et al. (44). (d) Analysis of ability of the chimeras to develop and express delayed-type hypersensitivity responses to contact sensitizer (2,4-dinitro-l-fluorobenzene [DNFB]) showed no apparent immunodeficiency of either chimeras to this form of immunization. Development of immunologic tolerance to DNFB, however, was grossly deficient in [B6 {arrow} AKR] chimeras but normal in [AKR {arrow} AKR], [B6 {arrow} B6], and [E(k) {arrow} AKR] chimeras. These findings indicate that full chimeras across major histocompatibility complex have considerable immunologic vigor even though primary immune responses that require histocompatibility between interacting cell types are initially defective.
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PMID:Humoral and cell-mediated immune responses in fully allogeneic bone marrow chimera in mice. 698 46

C3H/HeN mice administered BCG followed by lipopolysaccharide 14 days later released into their serum a cytotoxic factor for tumor cells and a factor that restored the anti-SRBC plaque-forming cell response of nude mouse spleen cells (helper activity). Gel filtration of serum containing the cytotoxic and the helper activities indicated that both factors exhibited an apparent m.w. of 125,000 to 150,000. The helper activity was also found at lower m.w. (60,000 and 13,000) suggesting the possibility that this factor existed in aggregated forms. Gel filtration of ammonium sulfate (40 to 60% saturation) precipitated serum in a high ionic strength buffer (1.6 M NaCl) resulted in shifts in the apparent m.w. of both factors. The cytotoxic factor now exhibited a m.w. of 55,000. The helper activity eluted with an apparent m.w. of 13,000, and thus was clearly separated from the cytotoxic factor. The helper activity was further shown to co-elute with macrophage-derived lymphocyte activating factor (LAF). This as well as other data represent the first demonstration of in vivo produced LAF.
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PMID:Separation of a serum-derived tumoricidal factor from a helper factor for plaque-forming cells. 698 7

Experiments were performed to investigate the role of adherent (A) cells in graft-versus-host (GVH)-induced immunosuppression. GVH reactions (GVHR) were induced in adult F1 hybrid mice by intravenous injections of parental lymphoid cells. Spleen cells (SC) from mice experiencing a GVHR (GVH mice) were stimulated with phytohaemagglutinin (PHA), concanavalin (Con A), and lipopolysaccharide (LPS). SC taken in the early phase of the GVHR (early GVHR) responded normally to LPS but did not respond to PHA and Con A. SC taken in an advanced phase of the GVHR (advanced GVHR) did not respond to PHA, Con A, or LPS. The influence of A cells from GVH mice (GVH-A cells) on the response of normal non-adherent cells to sheep erythrocytes (SRBC), PHA, and LPS was investigated. A cells from early GVHR, used in appropriate numbers, stimulated the responses to SRBC and to PHA; in excess they inhibited both responses. They had no effect on the response to LPS. A cells from advanced GVHR, even in low numbers, suppressed the responses to SRBC, PHA and LPS. The lymphoregulatory activities of GVH-A cells seemed to be mediated by soluble factors. The results indicate that the GVHR evokes complex non-specific regulatory interactions between A cells and lymphocytes.
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PMID:Role of adherent cells in graft-versus-host-induced suppression of the humoral immune response. 700 87

Daily gastric intubation of lipopolysaccharide (LPS)-responsive C3H/HeN, BALB/c, and Swiss mice with SRBC for 2 wk resulted in oral tolerance, whereas similarly treated LPS-nonresponsive C3H/HeJ mice gave splenic anti-SRBC PFC responses, including the IgA isotype, after systemic challenge with antigen. Oral tolerance in LPS-responsive C3H/HeN mice was due to T suppressor (Ts) cells because significant Ts cell activity was demonstrated in both Peyer's patches (PP) and spleens of these animals. On the other hand, T cells from PP and spleens of identically treated C3H/HeJ mice exhibited mainly T helper cell activity. Prior treatment of PP or spleen cell preparations from tolerant C3H/HeN mice with anti-Lyt-2.1 resulted in good in vitro anti-SRBC PFC responses, especially IgA isotype responses in PP cell cultures. These results indicate that oral administration of a thymic-dependent antigen (SRBC) to LPS-responsive mice induced a Ts cell population in PP, which, after migration to peripheral lymphoid tissue (e.g., spleen), suppressed responses to systemically administered antigen. LPS-nonresponsive mice lack this Ts cell pathway and continually respond to oral administration of antigen.
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PMID:Lack of oral tolerance in C3H/HeJ mice. 703

Pretreatment of mouse splenocytes with Shigella lipopolysaccharide and concanavalin A followed by 50 ng/ml of cimicifugoside resulted in a 69% and 31% inhibition of blastogenesis compared to controls. The plaque forming colony assay using sheep erythrocytes (SRBC) showed a decreased number of plaque forming colonies after exposure of the splenic cells to 1 microgram/ml of cimicifugoside. Cimicifugoside, 0.1 mg/mouse i.p. suppressed the anti-SRBC response in the plaque forming assay. The major inhibition of the antibody response occurred when cimicifugoside was administered 1 day before the primary immunization with SRBC. The delayed type hypersensitivity to picryl chloride was suppressed after i.v. administration of cimicifugoside, 1.0-2.0 mg/mouse. The immunosuppressive activity of cimicifugoside is preferentially directed toward B-cell function with larger doses being required for suppression of T-cell function.
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PMID:The immune response of splenic lymphocytes after cimicifugoside treatment in vitro and pretreatment in vivo. 727 79


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