Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024141 (systemic lupus erythematosus)
 44,322 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A patient with microvascular thrombosis and thrombocytopenia was found to have a high-titre lupus anticoagulant. The biological effects of the patient's lupus anticoagulant were studied using whole patient serum and plasma. Staph Protein A eluate, and affinity-purified lupus anticoagulant. The latter was isolated by immunoadsorption of serum onto cardiolipin/phosphatidylserine/cholesterol liposomes. Each source of lupus anticoagulant demonstrated 'anticoagulant' activity, defined as prolongation of a modified kaolin clotting time, and contained antibody which bound to endothelial monolayers. Each interfered with thrombin-mediated prostacyclin release from endothelial cells, but had no effect on arachidonate-induced prostacyclin release. In addition, the lupus anticoagulant selectively blocked platelet aggregation in response to thrombin, but not in response to arachidonate, ADP or epinephrine. Lupus anticoagulant also reduced thrombin-stimulated shifts in cytosolic calcium. Thrombin-mediated membrane inositol metabolism and total thrombin binding to endothelium were unaffected by lupus anticoagulant, and another endothelial anticoagulant function related thrombin binding. Protein C activation by thrombomodulin, was not altered. We conclude that the binding of lupus anticoagulant to endothelial cells and platelets does not prevent all thrombin signalling events, but does interrupt prostacyclin production.
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PMID:Lupus anticoagulant induces a selective defect in thrombin-mediated endothelial prostacyclin release and platelet aggregation. 249 19

A radioimmunometric technique for the detection of autoantibodies to liver membrane antigens has been developed using Alexander cells, a human hepatocellular carcinoma cell line. After incubation of Alexander cells with serum, antimembrane antibodies were detected by addition of 125I-labeled Protein A. Binding ratios in 15 children with uncontrolled autoimmune chronic active hepatitis and in seven children with primary sclerosing cholangitis were significantly higher than in 18 age-matched normal controls. Nine patients with inactive autoimmune chronic active hepatitis, 13 with alpha 1-antitrypsin deficiency and five with fulminant hepatic failure had ratios similar to controls. In nine patients with Wilson's disease, there was a modest but significant increase in binding ratio. In four children with autoimmune chronic active hepatitis, binding ratios fell during effective immunosuppressive therapy. Sera from patients with systemic lupus erythematosus or rheumatoid arthritis gave normal results, excluding that binding derives from Fc-mediated immune complex capture. A positive correlation was found between Alexander cell binding values and anti-liver-specific protein antibody titers, suggesting that the two assays detect antibodies against shared antigenic determinants. The Alexander cell assay is a simple, rapid and sensitive technique to detect antibody to liver cell membrane antigens.
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PMID:Detection of anti-liver cell membrane antibody using a human hepatocellular carcinoma cell line. 253 48

Non-reactive SLE sera in an ELISA for anticardiolipin antibody (aCL) retested positive in the immunoassay when the sera were first heat-inactivated at 56 degrees C for 30 minutes. This was not a false positive phenomenon since the positive ELISA reactivity of the heated SLE sera was markedly reduced by inhibition with the cardiolipin antigen. Furthermore, the heat-potentiated ELISA reaction was abolished by prior IgG depletion of the SLE sera with Protein A preparation. The unmasked aCL in the heat-treated SLE sera also exhibited selective binding in ELISA to other negatively-charged phospholipids, namely phosphatidylserine and phosphatidic acid but not against either phosphatidylcholine or phosphatidyl-ethanolamine. The data strongly indicate an interaction between antiphospholipid antibodies and heat-sensitive serum component(s), a reduction of the latter resulting in the ELISA detection of the autoantibody.
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PMID:Detection of antiphospholipid autoantibody in systemic lupus erythematosus is temperature-dependent. 261 88

Protein A, a cell wall protein found in bacterial strains of Staphylococcus aureus, has been extensively used in the analysis and purification of immunoglobulins and immune complexes. By binding protein A to microparticulate silica (high performance liquid affinity chromatography, HPLAC), a rapid and efficient chromatographic system was obtained for the separation and analysis of circulating immune complexes. The method was applied to the separation of artificial immune complexes as well as to plasma samples from patients with immune complex associated diseases such as SLE and RA. It was possible to distinguish certain subpopulations of circulating immune complexes by performing pH gradients on the protein A silica HPLAC column.
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PMID:Profiling of circulating immune complexes by high performance liquid affinity chromatography (HPLAC) on a protein A-silica matrix. 282 76

The lymphokine, interleukin 2 (IL-2), is an important modulator of cell-mediated immune (CMI) responses. We report here the detection of an inhibitor of IL-2 in normal sera by measuring the inhibition of thymidine incorporation in IL-2 dependent murine CTLL cells. The inhibitor, partially purified by Sephacryl S-200 gel filtration, eluted with the 60,000-70,000 mol. wt fraction. The factor was destroyed at 56 degrees C for 30 min and did not bind to Protein A Sepharose, suggesting that it is not an immunoglobulin G. Of 26 normal sera tested, 23 had significant levels of the inhibitor. Since connective tissue diseases are often associated with deficient CMI responses, we examined the levels of IL-2 inhibitor in 26 systemic lupus erythematosus (SLE) and 22 rheumatoid arthritis (RA) patients. Only 8 SLE and 12 RA patients had normal levels of the inhibitor. Of the 18 SLE patients with low or undetectable levels, 15 had clinically defined active disease and of the eight with normal levels, three had active disease. The decrease in the IL-2 inhibitor level did not correlate either with steroid or cyclophosphamide treatment or with serum levels of DNA binding and C3. These data suggest that the function of the inhibitor is to control IL-2 activity under normal conditions. Decreased levels of the IL-2 inhibitor in these patients might be explained either as a reduced requirement of this regulatory protein secondary to decreased IL-2 production or a defect of the cells responsible for the production of both IL-2 and its inhibitor.
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PMID:Decreased interleukin 2 inhibitor in sera of patients with autoimmune disorders. 379 99

Abnormally high levels of activity (BA) of immunoglobulins (Igs) to membranes containing TSH receptors were observed in patients with Graves' disease. The assay to detect such BA used guinea pig fat as the membrane source. [125I]Protein A was used to develop the binding antibodies (in serum or IgG). The assay was able to detect specific BA in microgram quantities or less of IgG in about 50% of the sera of patients with Graves' disease. The presence or amount of serum BA did not correlate consistently with either the presence in serum of TSH binding inhibitory Ig or the clinical estimate of thyrotoxicity in Graves' disease. High levels of BA were frequently found in sera of patients with other autoimmune diseases, such as Hashimoto's thyroiditis, rheumatoid arthritis, mixed connective tissue disease, and systemic lupus erythematosus. However, BA found in the latter disorders frequently was positive not only when using fat cell membranes but also when using liver kidney, or skeletal muscle membranes. The assay may detect a heterogeneous population of Igs binding specifically to membranes and may reflect a general state of autoimmunity.
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PMID:Membrane-binding antibodies in patients with Graves' disease and other autoimmune diseases. 612 89

It has recently been reported that many immunological abnormalities including the presence of TSH-receptor antibody (TRAb) were found in Graves' disease (GD). Circulating immune complexes (CIC) have also been detected in the serum of patients with GD as observed in systemic lupus erythematosus, which is thought to be a typical model of immune complex disease. The role of CIC in pathogenesis of hyperthyroidism, however, remains to be elucidated. Therefore, to clarify pathophysiological functions of CIC in GD, the levels of it in those patients were compared with their symptoms, those of TRAb, and lymphoblastogenesis (LBG) induced by phytohemagglutinin (PHA), concanavalin A (Con A), and pokeweed mitogen (PWM). The subjects were forty patients with GD without any medication, one hundred and nine patients with GD on medication with methimazole (MMI), and fifteen healthy volunteers. CIC was measured by three different methods; polyethyleneglycol precipitation method (PEG), Clq binding assay (Clq), and Protein A binding assay (PA). The normal range was estimated with the mean plus or minus two times the standard deviation of normal controls. In untreated GD, CIC determined by PEG, Clq and PA widely distributed from normal range to high levels. The positive rates of CIC determined by PEG, Clq, PA, and any one method of these three were 17.5%, 22.5%, 30.0% and 52.5%, respectively. LBG using incorporation of tritiated thymidine showed the decreases in PHA and Con A, and the increases in PWM in patients with GD. The positive rates of CIC determined by PEG and PA were significantly higher in patients without goiter or with small one than those with large one (p less than 0.05). CIC measured by all three of PEG, Clq and PA showed negative correlation with TRAb significantly (p less than 0.05, p less than 0.01, p less than 0.01, respectively). On the other hand, CIC measured by Clq showed significant negative correlation with serum thyroxine concentration (p less than 0.01). The levels of CIC, TRAb and PWM-induced LBG decreased following the tapering dose of MMI sufficient to keep patients in euthyroid state. In consequence, there were no longer any correlations between CIC and TRAb after thyroid function was normalized. These observations suggest that CIC's which have huge molecular weight or have ability to bind Fc receptor on K cell, macrophage, neutrophil, and other immune cells may be one of the factors to inhibit the goitrogenic action of TRAb, and that CIC's which have ability to activate the complement system may be one of the factors to inhibit the stimulation of secretion of thyroid hormone by TRAb.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[The role of circulating immune complexes in the pathogenesis of Graves' disease]. 632 60

A microplate-adapted enzyme linked immunosorbent assay (ELISA) for detection of C1q-binding immune complexes (IC) and aggregated IgG (delta IgG) is described. Purified human C1q was adsorbed to the wells of flat-bottomed microtiter plates and EDTA-treated serum samples were subsequently introduced. Bound IC was measured by use of alkaline phosphatase-labelled Protein A followed by the substrate para-nitro-phenyl-phosphate. A dose response was found for both delta IgG and BSA anti-BSA complexes, while variations in the concentration of monomer IgG did not affect the optical density. Elevated levels of IC were found in the majority of sera from patients with rheumatoid arthritis and SLE. The described C1q-PA-ELISA is a simple and inexpensive method for detection of C1q-binding immune complexes. The reproducibility is acceptable and the sensitivity is higher than for most IC-methods based on C1q-binding.
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PMID:Estimation of immune complexes by a microplate-adapted C1q-Protein A enzyme-linked-immunosorbent-assay (C1q-PA-ELISA). 633 38

A solid-phase assay for the detection of anti-F(ab')2 antibodies is described. Wells of microtiter plates are coated with F(ab')2, dilutions of sera are added, and IgG bound to the solid phase is detected using peroxidase-labeled Protein A. Anti-F(ab')2 antibodies were found in 61% of sera from patients with rheumatoid arthritis, 77% with subacute bacterial endocarditis , and 34% with systemic lupus erythematosus. Simultaneous analysis of these sera for immune complexes (IC), using modified Clq and monoclonal rheumatoid factor assays, showed that a correlation existed between anti-F(ab')2 antibodies and the levels of IC. Characterization of anti-F(ab')2 antibodies by inhibition and absorption experiments and by immunological and physical means indicated that they were similar to serum proteins described in the 1960s and designated pepsin agglutinators.
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PMID:Association of anti-F (ab')2 antibodies (pepsin agglutinators) with immune complexes as determined by enzyme-linked immunosorbent assays. 697 96

Protein A from Staphylococcus aureus, a cell wall protein with high affinity binding properties for IgG-type antibodies, has been labeled with peroxidase to form a stable immunohistological tracer molecule of relatively low molecular weight. It has been used for demonstration and titration of antinuclear antibodies in SLE sera on mouse liver sections in an indirect technique. The findings were consistent with those obtained by immunofluorescence and by staining with peroxidase-coupled anti-IgG. In contrast to immunofluorescence, the stained sections could be mounted and stored for documentation. In comparison, unspecific tissue adsorption and staining could be minimized by addition of glucose, galactose, and mannose as well as bovine serum albumine to the buffer containing Protein A-peroxidase.
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PMID:A new immunoenzyme tracer for immunohistology: peroxidase-labeled protein A. Its application for determination of antinuclear antibodies. 699 81


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