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Query: UNIPROT:P43026 (lipopolysaccharide)
 62,215 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

At low cell density, the proliferative response of B cells to lipopolysaccharide (LPS) is not detectable. We investigated under these experimental conditions the role of several cell populations on the LPS-induced B-cell proliferation. The addition to murine B cells of irradiated peripheral blood leukocytes (PBL) from the C3H/HeJ mouse strain, or of culture supernatants of these cells, efficiently restored a response to LPS. Similar results were also obtained with irradiated PBL from other mouse strains and from rabbits. The activities of the culture supernatants were not significantly modified when the PBL were depleted of adherent cells or of Thy-1.2 positive cells, thus suggesting that the active factors were secreted neither by T cells, nor by monocytes.
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PMID:Enhancement of murine B cell responses to lipopolysaccharide by supernatants of irradiated peripheral blood leukocytes. 387 9

Proliferative and differentiative signals controlling the in vitro IgM response by unprimed, affinity-enriched B cells were studied using conditions under which as few as 2,000 B cells stimulated by antigen-specific, Ia-positive, allogeneically restricted, T cell-derived helper factor (Hf) or the polyclonal activator lipopolysaccharide (LPS) yielded on the average 400 antibody-forming cells (AFC) by direct plaque assay. Antigen alone induces neither B cell proliferation nor differentiation into AFC. Proliferation but not differentiation into AFC is induced when affinity-enriched B cells are cultured in the presence of Ag and Hf or LPS but in the absence of nonantigen-specific, radioresistant, accessory (A) cells. For the induction of a complete Hf- or LPS-mediated AFC response, cultures must be reconstituted with A cells or the secretory product(s) of these cells. The antigen-specific response depends strictly on the presence of the Hf specific for the relevant antigen, regardless of the cell cycle state of cooperating B cells. The differentiative signal from A cells is due, at least in part, to the presence of a Thy-1.2-bearing population of cells. In the case of the LPS-mediated, but not the Hf-mediated response. A cells can be substituted by using supernatant derived from an interleukin 2-secreting T lymphoma cell line (EL4). In the presence of histocompatible Hf and B cells, histoincompatible A cells can still cooperate in the immune response. However, the degree of allogeneic restriction between incompatible Hf and B cells is markedly increased if both B cells and A cells are incompatible with Hf.
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PMID:Triggering of affinity-enriched B cells. Analysis of B cell stimulation by antigen-specific helper factor or lipopolysaccharide. I. Dissection into proliferative and differentiative signals. 617 41

Two mouse monoclonal antibodies to chicken immunoglobulin VH-associated idiotypes (Id), CId-1 and CId-2, were used as probes for Id determinants on mouse T cells. CId-1, which recognized chicken antibodies to N-acetyl glucosamine (NAGA), and approximately 0.4% of chicken T lymphocytes also reacted with approximately 0.2% of BALB/c splenic Thy-1.2+ cells. When enriched CId-1+ splenic T cells from NAGA-immune BALB/c mice were fused with the AKR thymoma BW 5147 cell line, 2 of 72 resulting hybrids, termed CId-1A and CId-1B, were reactive by indirect immunofluorescence with the CId-1 antibody. CId-1 determinants were expressed both in the cytoplasm and on the cell surface. Immunofluorescence studies revealed that both CId-1+ T cell hybrids were phenotypically identical: CId-2-/Ig-/Lyt-1+2-/Thy-1.2+/II-2d+/I-Ad-/I-Ak-/I-Jd+/I-Jk+. Incubation of CId-1B hybrid cells with concanavalin A or lentil lectin resulted in capping of the CId-1 determinant, whereas incubation with pokeweed mitogen, lipopolysaccharide, phytohemagglutinin, and wheat germ agglutinin had no effect on the cell surface distribution of the CId-1 molecule. Trypsin or pronase treatment resulted in the loss of detectable CId-1 determinant on the cell surface. Treatment of CId-1B cells with tunicamycin also reduced the immunofluorescence intensity of the surface CId-1 determinant, but had no effect on its cytoplasmic expression. CId-1 antibody-induced capping of the CId-1 marker did not affect the surface distribution of Lyt-1, Thy-1.2, H-2d, I-Jd, or I-Jk molecules. Conversely, capping of I-Jd and I-Jk determinants did not alter the surface distribution of CId-1. These results suggest that the CId-1 determinant is on a glycoprotein that is not physically linked to the Lyt-1, Thy-1.2, H-2d, I-Jd, and I-Jk molecules. The clonal restriction of CId-1 expression by T cells suggests that the CId-1+ molecule could be a T cell antigen receptor.
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PMID:T cell hybrids that express a VH idiotope-related determinant on a glycoprotein distinct from H-2, Thy-1, and Lyt-1 molecules. 619 22

In the absence of specific antigen stimulation, nonspecific killer cells were induced by culturing C57BL/6 lymph node or spleen cells with interleukin 2-containing supernatants. These supernatants were obtained from stimulation of either rat spleen cells with concanavalin A or a variant of the T cell lymphoma, EL4 (H-2b) with phorbol myristic acetate. The ability of the EL4 supernatant to induce nonspecific killer cells was abrogated by absorption with an interleukin 2-dependent T cell line or by concanavalin A-stimulated spleen cell blasts, but not by lipopolysaccharide-stimulated spleen cell blasts or by a non-interleukin 2-producing EL4 line. Partially purified interleukin 2 from EL4 supernatants could also support nonspecific killer cell induction. The induction of cytolytic cells by interleukin 2 is sensitive to gamma-irradiation and has a D omicron of 120 rad. The nonspecific killer cells induced are likely cytotoxic T lymphocytes; the majority of the precursor and effector cells bear the Thy-1 alloantigen marker. These nonspecific killer cells killed a broad spectrum of target cells, including concanavalin A- and lipopolysaccharide-induced splenic blasts of syngeneic or allogeneic mice, a syngeneic tumor, and a cloned allogeneic cytotoxic T cell line. The frequency of precursors for nonspecific killer cells in C57BL/6 lymph node and spleen cells are 1/7000 and 1/12,000, respectively. Clonal analyses revealed that these nonspecific killers exhibit heterogeneity with respect to their target cell specificities. The induction of nonspecific killers by interleukin 2-containing supernatants is partially dependent on nylon wool-adherent cells; in antigen-stimulated cultures the most specific killer cells were obtained from cultures in which nylon wool-nonadherent lymph node responder cells were stimulated with nylon wool-nonadherent allogeneic splenic stimulator cells that were treated with anti-Thy-1 antibody and complement. The relevance of these findings with respect to the frequencies and fine specificities of cytotoxic T lymphocytes generated in interleukin 2-supplemented cultures is discussed.
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PMID:Activation of nonspecific killer cells by interleukin 2-containing supernatants. 619 16

In vitro primary antibody responses of spleen cells can be suppressed in a dose-dependent manner by the addition of bond marrow cells (BMC). This suppression was not abrogated by treatment of BMC with anti-Thy 1, anti-Lyt nor with anti-I-J antisera and complement. Furthermore, preculture of BMC with the synthetic thymic pentapeptide (TP5) or Soluble Thymic Factor (STF) before anti-Thy-1 treatment was similarly ineffective in removing the suppressor cell activity. Similarly, treatment of BMC with polyvalent anti-immunoglobulin serum or anti-Ia antiserum and complement failed to remove the suppressor activity. However, preparations of anti-H-2 and anti-stem-cell antisera were capable of significantly decreasing the suppressive ability of BMC. BMC were also shown to be capable of suppressing antibody responses induced by the polyclonal activators dextran sulphate (DxS), lipopolysaccharide (LPS) and purified protein derivative from tubercle bacilli (PPD). The non-specificity of this suppressor coupled with the absence of well-defined antigen on its surface may suggest that this cell represents a basic level of immune regulation.
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PMID:The immunoregulatory role of bone marrow. III. Further characterization of the suppressor cell and its mode of action. 621 8

The objective of this study was to determine whether mature thymic-derived T-lymphocytes were required for streptozotocin (SZ)-induced insulitis. C57BL/KsJ male mice were immunocrippled by thymectomy at 3 wk of age followed 1 wk later by lethal irradiation (1000 R) and hematopoietic reconstitution with syngeneic bone marrow (pretreated with anti-Thy 1.2 antiserum and complement to eliminate mature T-lymphocytes). As a control for the systemic effects of lethal irradiation itself, thymus-intact males were also irradiated and reconstituted with anti-Thy-1.2-treated marrow cells. This latter treatment resulted in a reconstitution of functional T-lymphocytes. Independent of the presence or absence of functional T-lymphocytes, irradiation extensively damaged the testes and produced at least a 50% reduction in plasma testosterone levels. In such effeminized males, the hyperglycemic response following 6 daily injections of SZ (35 mg/kg) was reduced in comparison to unirradiated males. Pancreatic insulin content was reduced 50% in both thymus-intact and thymectomized groups receiving lethal irradiation and SZ treatment; this correlated with histologic findings of small, beta-cell-depleted islets. Focal leukocytic infiltrates of the exocrine pancreas were induced by the irradiation. Streptozotocin-induced insulitis was also observed regardless of the presence (in thymus-intact mice) or absence (in thymectomized mice) of phytohemagglutinin-responsive T-lymphocytes. Both groups exhibited intact B-lymphocyte function as measured by proliferative responsiveness to lipopolysaccharide. Severe immunosuppression of both T- and B-lymphocyte function was produced by subcutaneous injection of hydrocortisone into thymectomized mice 48 h prior to initiation of SZ treatments. This treatment prevented SZ-induced beta-cell necrosis and eliminated lymphocytic infiltrates in the endocrine and exocrine pancreas. We conclude that functional (mature) T-lymphocytes are not required to mediate the beta cytotoxicity of multiple low doses of SZ in inbred strains in which insulitis accompanies islet destruction. The ability of hydrocortisone to protect beta-cells from the direct cytotoxic action of SZ as well as to eliminate leukocytic infiltration in the pancreas would support the hypothesis that insulitis is a consequence of beta-cell destruction, in this model, rather than its cause. DIABETES 32:148-155, February 1983.
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PMID:The effect of immunosuppression on streptozotocin-induced diabetes in C57BL/KsJ mice. 621 26

It has been reported (Contemp. Top. Immunobiol. 1974. 3:41) that allotype-specific T suppressor cells can be induced after monoclonal anti-allotype treatment of neonatal (BALB/c X SJL)F1 (Igha/b) mice. Here we show that (BALB/c X CB20)F1 adult-derived spleen cells (SC) are, by contrast, potently suppressed by monoclonal allotype-specific reagents, (when transferred into irradiated BALB/c recipients) in the absence of primary T suppressor cell induction. Such suppression is only induced in activated B cells [exposed to lipopolysaccharide or sheep red blood cells (SRBC)], and is probably dependent on the isotype of the anti-allotype sera administered. For example, two independently produced IgG1 monoclonal reagents raised against the Igh-1b allotype were poorly suppressive or nonsuppressive, whereas an IgG3 and an IgG2a monoclonal antibody induced a 90% suppression of the target allotype in transferred adult SC. It was found that suppression was not due to a depletion of antigen-specific T cell help since: (a) the addition of SRBC-educated T cells did not break suppression and (b) suppressed SC were as good a source of T cell help as normal SC, in the response of virgin or memory B cell (Thy-1-depleted) responses to SRBC in vivo. Suppression was maintained in suppressed cells which had been rechallenged with SRBC after transfer into a second irradiated recipient, but was not induced in normal SC when these were admixed with an equal number from this suppressed SC population. These findings point to a possible mechanism for the regulation of B cell expression, through the formation of an antibody-Ig receptor complex at the surface of the B lymphocyte. After complexing the target cell is either deleted or inactivated. The response to SRBC was reduced or ablated for at least 70 days after treatment with a single dose of anti-allotype serum.
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PMID:Antibody-mediated allotype suppression in adult mice: the role of antigen, effector isotype and regulatory T cells. 623 17

The effect of fractionated total lymphoid irradiation (TLI) on the maturation of B cells was examined in mice. At various times after irradiation of the mice, their spleen cells were tested for the mitogenic responses to dextran sulfate and lipopolysaccharide. In parallel the cells were stained with fluorescent anti-Thy-1 and various anti-Ig antisera, and were analyzed on a fluorescence-activated cell sorter (FACS). By comparison with normal spleen cells the cells of TLI-treated mice gave a high response to dextran sulfate and a low response to lipopolysaccharide. FACS analysis revealed that TLI-treated spleen contains elevated numbers of B cells bearing high IgM and low IgD on the surface. The B cells of TLI-treated mice retained these immature characteristics even two to four months after the last irradiation. These findings indicate that TLI causes a longlasting blockage in B cell maturation processes.
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PMID:Modulation of B and T cell subsets in mice treated with fractionated total lymphoid irradiation. I. Blockage of differentiating B cell pathways. 633 50

To further our understanding of the role of host immunity in the development of lymphoid neoplasia, groups of germfree BALB/c nude and nu/+ mice were either followed unmanipulated or were treated, beginning at birth, with anti-mu, normal goat IgG or with lipopolysaccharide (LPS). The survival and development of neoplasia of all groups of animals were monitored up to 2 yr. Nude mice, under germfree and specific pathogen-free (spf) conditions, had a higher incidence of lymphoid neoplasia and reduced survival when compared to nu/+ littermates. The incidence of lymphoid tumors in nude mice under spf or germfree conditions was 7.2 and 8.7%, respectively, in comparison to 0% in nu/+ animals. Treatment of germfree nude mice with anti-mu, but not with goat IgG, increased the incidence of lymphoid tumors to 39%. Anti-mu did not significantly change the incidence of lymphoid neoplasia in nu/+ animals. Treatment of nu/nu and nu/+ mice with LPS, however, led to a several-fold increase in the appearance of neoplasia, to values of 25.4% in nude and 10% in nu/+ mice. Lymphoid neoplasia found in either unmanipulated, anti-mu, or IgG-treated germfree or spf mice included Thy-1.2+, surface IgM+, and IgG+ tumors. In contrast, all the lymphomas found in LPS-treated mice were surface IgM+. Thus, whereas LPS may have generated a relatively homogeneous group of tumors, anti-mu may have randomly increased the normal incidence of spontaneous tumors. Moreover, although there was significant variation in the histologic appearance of tumors, both within treatment groups as well as in different areas of the same animal, only LPS-treated mice were regularly noted to have distant nonlymphoid involvement, with lesions found in liver, lung, and kidney. In contrast, the incidence of nonlymphoid neoplasia was similar and was less than 2.5% in all groups.
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PMID:Anti-mu induces lymphoma in germfree congenitally athymic (nude) but not in heterozygous (nu/+) mice. 641 85

Animals treated with formalinized Candida albicans manifest depressed cellular immune activity. Splenocytes from mice treated with as little as 14 micrograms of this material exhibited significantly reduced responses to the T cell-dependent mitogens phytohemagglutinin and concanavalin A. On the other hand, the B lymphocyte-dependent response to bacterial lipopolysaccharide was normal in these cultures. Splenocytes from treated mice were capable of actively suppressing the T cell- (but not B cell-) dependent proliferative response of normal cells. Analysis of splenocytes from Candida-treated mice showed that the suppressor cell is adherent to glass wool, is not adherent to Sephadex G-10, does not phagocytize carbonyl iron, is not susceptible to treatment with anti-Thy-1 plus C, but does bind specifically to anti-immunoglobulin- (anti-Ig) coated dishes. The adherence to the anti-Ig-coated dishes was not due to the simple attachment of Fc receptor-bearing lymphocytes, because dishes coated with the F(ab')2 fragment of rabbit antimouse IgG bound the suppressor cell. These results suggest that the active Candida-induced suppressor cell is composed, at least in part, of surface Ig-bearing B lymphocytes.
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PMID:Studies on the cellular nature of Candida albicans-induced suppression. 660 Jan 88


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