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)

The effects of 3-acetyldeoxynivalenol (3-AcDON) on mitogen-induced lymphocyte proliferation and antibody production were studied in male CD-1 mice exposed to 0, 2.5, 5 or 10 ppm 3-AcDON in the diet for 35 days. Mitogen-induced lymphocyte proliferation and T-cell-independent antibody responses to dinitrophenyl-ficoll or Escherichia coli were not altered by dietary exposure to 3-AcDON. The T-cell-dependent antibody response to sheep red blood cells was increased in the group fed 10 ppm 3-AcDON. In vitro, 3-AcDON inhibited lymphocyte proliferation in a dose-dependent manner. Inhibition was observed when the toxin was present during the first 8 hr in phytohaemagglutinin-stimulated cultures and during the first 24 hr in lipopolysaccharide-stimulated cultures. This suggests that 3-AcDON blocks an early step in lymphocyte activation. This inhibition was not restored by thiol reducing agents (dithiothreitol, L-cysteine or 2-mercaptoethanol). Similarly, the addition of lymphokines, including interleukin-1 or interleukin-2, did not alter the inhibitory effects of 3-AcDON. These results suggest that the in vitro effects of 3-AcDON may not reflect its in vivo immunotoxicity. However, 3-AcDON may serve as a chemical probe for examining the activation process of lymphocyte proliferation.
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PMID:Immunological responsiveness of mouse spleen cells after in vivo or in vitro exposure to 3-acetyldeoxynivalenol. 360 79

We describe here several improvements in the method we originally developed to prepare mitotic chromosomes from peripheral blood of laboratory mice. In addition, we have tried several methods to improve metaphase yield from lymphocytes of the inbred strain DBA/2J, which respond poorly to phytohemagglutinin. The yield of mitoses from DBA/2J cells cannot be improved by enhancing T-cell response using interleukin-2 or by using a different T-cell mitogen, concanavalin A. Metaphase yield from peripheral blood cells of DBA/2J mice can be improved significantly by adding lipopolysaccharide to cultures, probably stimulating B-cell as well as T-cell proliferation.
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PMID:An improved method for preparing G-banded chromosomes from mouse peripheral blood. 362 12

The effect of cimetidine treatment on the generation of interleukin-1 (IL-1) and interleukin-2 (IL-2) was studied in 11 duodenal ulcer patients. The results obtained were compared with those for untreated healthy subjects. The drug was administered intravenously in a dose of 200 mg four times a day for 8 days. The investigations were performed before, during and 1 wk after cimetidine therapy. IL-1 generation was determined by the ability of supernatants from 2-day cultured adherent cells stimulated by lipopolysaccharide to enhance proliferation of PHA-stimulated mice thymocytes. IL-2 generation was determined by the ability of supernatants from 2-day cultured, PHA-stimulated mononuclear cells to proliferate autologous 17-day cultured T cells. In all ulcer patients IL-1 generation diminished during cimetidine treatment (P less than 0.005). It continued to decrease in 4 subjects and increased in the other 7 ones following drug withdrawal. All the values were higher than those in healthy controls. IL-2 activity in ulcer patients was similar to that in healthy subjects and it increased significantly in all ulcer patients following the onset of the treatment (P less than 0.005) and decreased nearly to the initial values 1 wk after termination of the treatment (P less than 0.005). The present studies indicate that cimetidine, a selective histamine H2-receptor antagonist, deeply changes mechanisms of immunoregulation in patients with duodenal peptic ulcer.
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PMID:Changes in the interleukin-1 and interleukin-2 generation in duodenal ulcer patients during cimetidine treatment. 387 51

Conditions for production and detection of a monocyte-derived interleukin-1 like accessory factor were investigated. The production of the accessory factor was not increased quantitatively by changes in monocyte concentration or incubation times. Lipopolysaccharides stimulated monocytes to accessory factor production in a broad range of concentrations, and it was active even in concentrations below the often registered endotoxin contamination of commercial culture media. Thus, to avoid unintended monocyte stimulation culture conditions should be endotoxin-free. The accessory factor was heat-labile, had a MW between 10 and 40 K, was co-mitogenic to PHA-stimulated monocyte depleted cells and it did not support the growth of an interleukin-2 dependent cell-line. Thus the factor shares characteristics with and might be identical to interleukin-1. The conditions previously defined for the demonstration of accessory effect of monocytes were also optimal for demonstration of interleukin-1 in supernatants from lipopolysaccharide stimulated monocyte cultures.
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PMID:A standardized human T-lymphocyte proliferation assay for detecting soluble accessory factors from monocytes. II. Interleukin-1 production and detection. 387 22

Human T lymphocytes cultured in vitro for 5 days with Candida albicans purified polysaccharide (MPPS) produce and antigen non-specific inhibitor (nsINH) which blocks cell proliferation when added at the beginning of the culture. The antigen presenting function of antigen pulsed adherent cells (macrophages) is significantly impaired by incubation in nsINH. Further analysis shows that nsINH blocks the production of interleukin-1 both from human mononuclear cells stimulated with lipopolysaccharide. Furthermore, the production of interleukin-2 (IL-2) is also suppressed when MPPS stimulated cells are cultured in presence of nsINH. However nsINH does not affect the appearance of IL-2 responsive cells as the addition of gibbon IL-2 to the culture fully reverses the suppressive effect of nsINH on blast transformation.
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PMID:A non-specific inhibitor produced by Candida albicans activated T cells impairs cell proliferation by inhibiting interleukin-1 production. 389 Nov 66

In this work we study the role of subsets of human T cells, detectable by the OKT series of monoclonal antibodies, in the production of and the response to the lymphokine interleukin-2 (Il-2) during the course of an allogeneic cytotoxic T lymphocyte response in vitro. The results obtained establish that the Il-2 producer cells reside within the OKT4 positive T cell subset. Once produced, Il-2 mediates the clonal expansion of alloantigen-activated cytotoxic T killer cells which reside in the OKT8 positive T cell subset. Il-2 appears to have no mitogenic activity on the activated OKT4 positive T cells which produce the lymphokine. In order to release Il-2, the OKT4 positive T cell requires a stimulus, such as allogeneic cells or the lectin phytohaemagglutinin A (PHA). Macrophages are also required for Il-2 production, but the macrophage requirement can be bypassed by a soluble macrophage product as found in supernatants of lymphocyte cultures stimulated with lipopolysaccharide (LPS), the biological activity presumably representing Interleukin-1 (Il-1).
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PMID:Interactions of human T cell subsets during the induction of cytotoxic T lymphocytes: the role of interleukins. 621 93

Recent studies have provided evidence that deficient interleukin-2 (IL-2) production by helper T cells contributes to the impaired T-cell-mediated functions observed in aged mice. Since most of these responses depend upon the presence of macrophages, a deficit in the functional capacity or in cell cooperation of macrophages may result in a decrease in immune reactivity. We found in the present study, that in vitro the cytostatic activity of macrophages from aged C57BL/6 (B6) mice is affected only slightly, but that in vivo their number increases with age. The synthesis of IL-1 is reduced when macrophages from aged mice are stimulated in vitro by lipopolysaccharide, but addition of exogenous IL-1 apparently does not restore either the mixed lymphocyte reaction or cytotoxic T lymphocyte generation. Co-cultures of young splenic macrophages with aged T lymphocytes do not restore to normal level the impaired proliferative response to T mitogens of aged B6 mice, but aged splenic macrophages provide a full accessory help for mitogenesis of young T cells. Thus, absorption of IL-1 by phytohemagglutinin-activated T cells is slightly altered in aged mice. IL-2 responsive T cells are not altered since exogenous IL-2 supply in vitro completely reconstitutes cytotoxic T lymphocyte generation after an allogeneic stimulation. Moreover, the number of Lyt 1+ cells is not modified in aged B6 mice. These results suggest that the impaired capacity of macrophages to release IL-1 and of blast T cells to bind IL-1 may contribute to the depression of cell-mediated immune reactivity associated with aging but also that the main defect is a functional lesion of IL-2 production by Lyt 1+ helper T cells.
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PMID:Interleukin-1 synthesis and activity in aged mice. 623 33

C6 glioma cells, and primary cultures of mouse astrocytes, stimulated with lipopolysaccharide (LPS) release an interleukin-1 like factor (IL-1) which enhances lectin-induced T-lymphocyte proliferation and promotes the release of interleukin-2 (IL-2) by ConA-stimulated thymocytes. In the present study, the glia maturation factor (GMF) was found not only to induce differentiation of glioblasts, but also to elicit the secretion of IL-1 like factors by cultured mouse astrocytes and their precursor cells. GMF was also effective in triggering IL-1 release by macrophages. Contamination of the 23 000 MW GMF preparation with LPS was excluded by the Limulus lysate assay and by using C3H/HeJ LPS-nonresponder mice whose glia and macrophages responded to GMF but not to LPS, by IL-1 release. Through its ability to induce glial differentiation and IL-1 release, GMF may represent an important endogenous signal, triggering both reactive gliosis and the development of an immune response within the central nervous system.
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PMID:Dual effect of glia maturation factor on astrocytes. Differentiation and release of interleukin-1 like factors. 660 46

The effect of insertion of plasma membrane components from lymphocytes responding to mitogens into the membranes of nonresponding cells using Sendai virus envelopes as vehicles was examined. T cells modified by B membranes were stimulated by lipopolysaccharide (LPS) to proliferate as well as to produce interleukin-2 activity. B cells modified by T membranes were stimulated by concanavalin A to proliferate and to produce interleukin-2 activity. B cells derived from C3H/HeJ LPS-nonresponder strain of mice, when modified by B membranes derived from the LPS-responder C3H/eb strain, acquired LPS responsiveness. These findings indicate that the inability of either T or B cells to respond to specific mitogens is due to the lack of suitable plasma membrane constituents and that by changing the membrane composition the lymphocytes can be endowed with new functions.
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PMID:Acquisition of mitogenic responsiveness by nonresponding lymphocytes upon insertion of appropriate membrane components. 698 63

Interleukin-2 (IL-2) has been proven to be a defective element in immune regulation in systemic lupus erythematosus (SLE). However, its course in time is unknown. We studied its production and cellular response in the peripheral blood cells of 30 SLE patients and 12 healthy subjects. In addition, we studied the spontaneous and lipopolysaccharide (LPS) induced production of IL-1, which have been found to be, respectively, increased and lowered in untreated SLE patients. Patients were studied at the outset, when still untreated, and at 1, 2, 6, 12, 18, and 24 months. At the outset, 18 had active disease and 12 were in remission. The decreased proliferative response of T cells to IL-2 and the deficient production of IL-1 upon LPS induction became normal after 6 months treatment, whereas the expression of high affinity IL-2 receptors took 18 months to become normal and the deficient production of IL-2 took 2 years. Despite clinical remission, the decreased capacity of T cells to absorb IL-2 persisted for 2 years. The effect of various prednisone dosages on the measured variables was evaluated. With intermediate doses of prednisone (20-45 mg), we observed the largest improvement in IL-2 production and in IL-1 production upon LPS stimulation. Higher doses of prednisone reduced also the spontaneous production of IL-1 and resulted in an increase in the expression of CD25+ cells. The addition of low doses of cytotoxic drugs (oral cyclophosphamide or azathioprine) resulted in an improvement in the capacity to absorb IL-2 and a reduction in spontaneous IL-1 production.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Longitudinal study on the production of and cellular response to interleukin-2 in patients with systemic lupus erythematosus. 748 81


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