Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.1.3.1 (alkaline phosphatase)
47,916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The binding of IL-2 and IL-3 to the factor-dependent cell lines CTB6 and 32D, respectively, was determined using biotinylated ligand detected by the addition of a streptavidin/alkaline phosphatase conjugate and amplified with a phosphatase amplification system. Binding of both ligands was detectable after incubation with as little as 20 fmol of ligand and could be inhibited with a 10-fold molar excess of nonbiotinylated ligand. No binding was observed when biotinylated ligand was incubated with a receptor negative cell line (PC-12) and IL-2 was unable to compete with biotinylated IL-3 binding to 32D cells, further demonstrating specificity. These studies indicate that biotinylated ligands can be used as a nonradioactive method to detect specific, high-affinity cell surface receptors.
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PMID:A colorimetric method for detection of specific ligand binding. 132 34

Interleukin-5 (IL-5) was shown to enhance, in a dose-dependent fashion, the expression of alkaline phosphatase (APase) activity in splenic B cells stimulated with dextran sulphate (DXS). The potentiating effect of IL-5 was still more evident when assayed in large B cells than in small resting B cells, whereas IL-2, IL-4 and IL-6 were devoid of activity. Concomitant with increased APase expression, cell-cycle analysis by flow cytometry showed that large B cells in the early G1 phase were stimulated by IL-5, in conjunction with DXS, to enter G1B and to progress further through S and G2/M. A phosphorylation-dephosphorylation pathway could, thus, be involved in IL-5 transmembrane signalling.
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PMID:Interleukin-5 increases the expression of alkaline phosphatase activity in murine B lymphocytes. 138 38

Membrane receptors specific for IgD (IgD-R) have been identified on murine CD4+ and human CD4+ and CD8+ T lymphocytes. Up-regulation of these IgD-specific receptors can be achieved by exposure of such T cells to various stimuli, including oligomeric or Ag cross-linked IgD, IL-2, IL-4, and T cell mitogens, such as PHA. Previous studies with murine IgD-R+ splenic T cells and IgD-R+ T hybridoma cells have demonstrated the existence of soluble IgD-binding factors (IgD-BF) that are shed or released into the medium in which these cells are grown. In our study, human peripheral blood T cells and IgD-R+ T hybridoma cells were examined for their ability to produce human IgD-BF. PHA stimulation of peripheral blood T cells results in their release of an IgD-specific factor with an apparent Mr of 70 kDa. IgD- Sepharose-purified IgD-BF was able to competitively inhibit rosetting of IgD-R+ T cells with IgD-coated RBC. Immunoblot assays in which alkaline phosphatase-conjugated human IgD myeloma protein was used as a probe, confirmed the IgD specificity of IgD-BF. An IgD-BF-specific mAb (LTB9) that also reacts with membrane IgD-R was produced after immunization of BALB/c mice with this factor. LTB9 was able to detect IgD-BF in the supernatants derived from human IgD-R+, tetanus toxoid-specific T hybridoma cells, H9-CEM1, and to stain membrane IgD-R by indirect immunofluorescence. Stimulation of H9-CEM1 cells with immobilized IgD resulted in up-regulation of membrane IgD-R expression, as measured cytofluorometrically with LTB9-stained cells, and potentiated release of IgD-BF from these cells. Finally, LTB9 as well as IgD-Sepharose, immunoprecipitated a 70-kDa protein from the lysates of biosynthetically labeled H9-CEM1 cells. Similar immunoprecipitation results were obtained with H9-CEM1-derived supernatants containing IgD-BF. Taken together, these results support the hypothesis that human T cell membrane IgD-R are released as soluble IgD-BF.
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PMID:IgD-receptor-positive human T lymphocytes. II. Identification and partial characterization of human IgD-binding factor. 154 18

Since our previous experiments suggested that glycosylation-inhibiting factor (GIF) is a phosphorylated derivative of a phospholipase inhibitory protein, we determined whether other well-known phospholipase inhibitors may have similar biological activities. The results showed that phospholipase A2 (PLA2) inhibitors, such as recombinant human lipocortin I and ONO-RS-082, could switch T cell hybridoma 12H5 cells from the formation of glycosylated IgE-binding factors (IgE-BF) to the formation of unglycosylated IgE-BF, whereas neomycin, a phospholipase C inhibitor, failed to affect the nature of IgE-BF formed by the cells. The minimum concentrations of lipocortin I and ONO-RS-082 required for switching the 12H5 cells to the formation of unglycosylated IgE-BF were comparable to or less than IC50 of the inhibitors for PLA2. The ability of partially purified GIF to switch the 12H5 cells to the formation of unglycosylated IgE-BF was markedly enhanced by treatment of the preparation with alkaline phosphatase. It was also found that lipocortin I and ONO-RS-082, but not neomycin, facilitated the generation of GIF-producing T cells. When spleen cells of ovalbumin (OVA)-primed BDF1 mice were stimulated with homologous antigen and the activated T cells were propagated by recombinant IL-2 in the presence of GIF, lipocortin I, or ONO-RS-082, T cells obtained in the cultures constitutively produced their own GIF. Antigenic stimulation of the T cells induced the formation of unglycosylated IgE-BF and GIF with an affinity for OVA.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of phospholipase A2 inhibitors on mouse T lymphocytes. I. Phospholipase A2 inhibitors exert similar immunological activities as glycosylation inhibiting factor. 253 36

Three cell lines of mature T cell origin established from patients with cutaneous T cell lymphoma-leukemia (CTCL) have been found to be constitutive producers of TCGF (L-TCGF). Biologically active L-TCGF can also be eluted from the plasma membranes of these cells. We have compared the biologic and biochemical properties of L-TCGF and TCGF derived from normal lymphocytes (N-TCGF). L-TCGF and N-TCGF share similar biologic activity: both support long-term growth of T cells that have undergone prior lectin or antigen stimulation, and have no effect on unstimulated T cells. However, L-TCGF is a more acidic (pI 4.5 vs 6.5 to 8.0) molecule than N-TCGF and elutes from DEAE-Sepharose at higher salt concentration (0.2 M NaCl vs 0.07 to 0.1 M NaCl). In addition, these two factors display differing mobilities on gel filtration. Treatment of L-TCGF with neuraminidase or alkaline phosphatase does not alter its pI, indicating that enzymatically vulnerable sialic acid or phosphate groups are not involved in the variation. The nature and significance of this biochemical variant remain unknown.
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PMID:A biochemical variant of human T cell growth factor produced by a cutaneous T cell lymphoma cell line. 698 Sep 38

K46J B lymphomas express a T cell costimulatory activity that is not inhibited by CTLA-4Ig, anti-B7-1, anti-B7-2, anti-intercellular adhesion molecule 1 or antibodies to heat stable antigen. In this paper we report that this costimulatory activity is mediated at least in part by 4-1BB ligand, a member of the tumor necrosis factor (TNF) gene family that binds to 4-1BB, a T cell activation antigen with homology to the TNF/nerve growth factor receptor family. A fusion protein between 4-1BB and alkaline phosphatase (4-1BB-AP) blocks T cell activation by K46J lymphomas in both an antigen-specific system and with polyclonally (anti-CD3) activated T cells. 4-1BB-AP also blocks antigen presentation by normal spleen cells. When the antigen-presenting cells express B7 molecules as well as 4-1BB ligand, we find that B7 molecules and 4-1BB-AP both contribute to T cell activation. These data suggest that 4-1BB ligand plays an important role in costimulation of IL-2 production and proliferation by T cells. The B lymphoma M12 expresses low levels of 4-1BB-L but can be induced to express higher levels by treatment of the B cells with cAMP, which also induces B7-1 and B7-2 in these cells. Thus cAMP appears to coordinately induce several costimulatory molecules on B cells.
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PMID:Role of 4-1BB ligand in costimulation of T lymphocyte growth and its upregulation on M12 B lymphomas by cAMP. 753 86

Primary biliary cirrhosis (PBC) is a chronic, progressive, cholestatic liver disease. Interleukin-1 beta (IL-1 beta) may play a role in the pathogenesis of PBC by contributing to altered immune function and fibrosis. Colchicine or methotrexate has some beneficial effects in the treatment of PBC, and also affects interleukin-1 (IL-1). Therefore, we prospectively studied the synthesis of IL-1 beta by peripheral blood mononuclear cells (PBMC) from 42 patients with PBC entered into a randomized, double-blind, double-dummy controlled trial of colchicine and methotrexate. PBMC obtained at entry, 6, 12, 18, and 24 months were stimulated to produce IL-1 beta with phytohemagglutinin (PHA), lipopolysaccharide (LPS), Staphylococcus epidermidis, recombinant IL-2, or mitochondrial antigen. Patients in the two treatment groups did not differ at entry in biochemical measures or liver histological stage. Over 24 months in both groups, serum bilirubin and histologic stage remained stable and alkaline phosphatase decreased significantly. For all patients, synthesis of IL-1 beta increased constitutively and in response to immune-mediated stimulants (PHA, IL-2, and mitochondrial antigen) but not the bacterial stimulants LPS or S epidermidis. Compared with levels of IL-1 beta at entry, PHA induced increases for patients treated with methotrexate (12, 18, and 24 months) or colchicine (18 and 24 months). At 24 months, IL-2-induced IL-1 beta synthesis was increased in patients treated with methotrexate, whereas S epidermidis-induced IL-1 beta was enhanced in colchicine-treated patients. Before treatment, IL-1 beta production did not relate to severity of disease except in response to S epidermidis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Synthesis of interleukin-1 beta in primary biliary cirrhosis: relationship to treatment with methotrexate or colchicine and disease progression. 763 20

Groups of BALB/c mice were treated with a sub-lethal dose (60 micrograms) of staphylococcal enterotoxin B (SEB) intraperitoneally and were sacrificed at 2, 5, 8, or 10 h post-injection. Organ, blood plasma and lymph node samples from these mice were analyzed. Plasma levels of urea, creatinine and alanine aminotransferase were significantly raised above normal by 5 h post-injection. However, alkaline phosphatase levels showed an erratic increase after toxin administration and, after administration of 10-40 microgramS SEB per mouse, were consistently at least 30% below normal levels at 24 h post-injection. Weight change was also monitored but found to be inconsistent. Lung, spleen and kidney samples appeared normal on histopathological examination, but liver samples showed minor polymorph infiltration and congestion. TNF-alpha, and IL-1 alpha levels in the plasma were raised by 8 h to picogram levels per ml of plasma, whereas IFN-gamma and IL-2 were raised by 2 h to nanogram levels per ml of plasma. Lymph node cells taken from mice treated with toxin were given a secondary stimulation with toxin in vitro. Although the response of the cells was lower than normal on assay at four days, a time response curve showed a peak in cell responsiveness to secondary stimulation with toxin at three days. These data indicate that biochemical markers and cytokine levels are affected by the administration of SEB to mice and may be used as indicators of toxicity.
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PMID:Staphylococcal enterotoxin B toxicity in BALB/c mice: effect on T-cells, plasma cytokine levels and biochemical markers. 764 Jun 77

This study describes the development of a sandwich enzyme immunoassay (ELISA) for rat soluble IL-2 receptors (sIL-2R) using a combination of monoclonal antibodies reactive with different epitopes on the rat IL-2R. Coating plates with NDS61 and NDS64 monoclonal antibodies produced similar dose-response curves when incubated with a standard sIL-2R preparation followed by biotinylated OX39, streptavidin-alkaline phosphatase and the substrate. Although normal rat serum inhibited the assay, the effects were more profound when NDS64 was used as the capture antibody and subsequent development of the assay was performed using NDS61. The intra- and interassay variations were typically less than 5%. This assay will be valuable for monitoring immune activation status in a variety of experimental models.
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PMID:Development of an enzyme immunoassay for rat soluble interleukin-2 receptors. 776 48

The purpose of this study was to compare, using cell blot analysis, the association of gingival tissue mononuclear cells (GTMC) isolated from lesions displaying histories of early-onset periodontitis (EOP; typically B-lymphocyte dominated) and gingivitis (typically T-lymphocyte dominated) with the B-cell stimulating cytokine, interleukin (IL)-4, and the T-cell stimulating cytokine, IL-2. Eleven EOP patients and 11 age- and gender-similar gingivitis control (GC) subjects participated. Gingival tissue adjacent to the alveolar crest normally removed during surgery was digested in collagenase-containing media and GTMC were isolated by density gradient centrifugation. Cells were separated into four aliquots. One was left unstimulated; the remainder were stimulated for 2 hours with Porphyromonas gingivalis outer membrane protein, mitogen Concanavalin A, or common antigen tetanus toxoid. Cells then were centrifuged onto transfer membranes and incubated in RPMI 1640 media for 6 hours to allow absorption of secreted cytokine. Membranes were treated with monoclonal anti-IL-2 or anti-IL-4, followed by a biotin-conjugated second layer, streptavidin-alkaline phosphatase and nitro blue tetrazolium/5-bromo-4-chloro-indolyl-phosphate (NBT/BCIP) color development. A higher percentage of GTMC from EOP patients were IL-2+ when stimulated with P. gingivalis compared with GTMC from GC patients (20 +/- 2% vs. 12 +/- 2%, P < 0.003). A higher percentage of non-stimulated GTMC from EOP patients produced IL-4 than from GC (22 +/- 4% vs. 6 +/- 3%, P < 0.00007), as well as when stimulated with P. gingivalis (22 +/- 3% vs. 13 +/- 2%, P < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Gingival cell IL-2 and IL-4 in early-onset periodontitis. 799 15


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