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)

The solid-phase C1q binding assay for circulating immune complexes has been evaluated. The assay provides a rapid, sensitive (detecting as little as 1 microgram of aggregated IgG) and reproducible procedure for the detection of immune complexes in biological fluids. Using artificially prepared immune complexes, the assay detects complexes at four-times antigen-excess. Gel filtration over Sepharose 6B showed that these complexes were distributed over a range of molecular weights from greater than 4 x 10(6) to 300,000 daltons. Using radiolabelled anti-BSA, antigen (BSA) could be detected in these complexes. Screening of gel-filtered SLE showed that the assay detects complexes of both high and low molecular weight, but does not detect all complexes in the SLE sera. Clinical studies showed that immune complexes are frequently found in the sera of patients with SLE and measurement of the concentrations of complexes provides a more sensitive index of disease activity than either serum C3 or C4 concentrations or DNA binding capacity. In patients with RA concentrations of immune complexes were generally higher in synovial fluid than serum, although a patient with systemic rheumatoid disease with hypocomplementaemia had an extremely high level of circulating immune complexes. The assay only infrequently detects circulating immune complexes in glomerulonephritis and in renal transplant recipients. It is concluded that the assay provides a useful clinical tool, but detects only a limited species of immune complexes. It can be used in the detection of antigens in complexes.
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PMID:Evaluation of the C1q solid-phase binding assay for immune complexes. A clinical and laboratory study. 9 1

Antinuclear antibodies (ANA) of the IgE class were studied in sera from patients with rheumatoid arthritis (RA), systemic lupus erythematosus (SLE) and healthy controls. Sixty per cent of 20 RA patients with neutropenia were found to have IgE granulocyte-specific (GS-)ANA, whereas only 16% of RA patients without neutropenia had IgE antibodies of similar specificity. About 5% in each group of RA patients had IgE organ-nonspecific (ON-)ANA. Eleven of 15 patients with active SLE and only 4 of 20 with inactive SLE had IgE ON-ANA. Sera from five patients with lupus nephritis all contained IgE ON-ANA. None of 100 sera from controls showed presence of IgE ANA. IgE ANA titres in RA and SLE patients correlated to the titres of ANA of the other four immunoglobulin classes. Gel filtration studies at neutral and acid pH of RA sera containing high titres of IgE GS-ANA indicated the presence of these antibodies in immune complexes. Studies of serum cryoprecipitates supported this conclusion. IgE ANA production may be of pathogenetic importance in RA and SLE by eliciting type-I reactions.
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PMID:The prevalence of IgE antinuclear antibodies in rheumatoid arthritis and systemic lupus erythematosus. 30 5

Hydroxyl radical, a prominent entity of reactive oxygen species, is known to modify cellular DNA and has been implicated in several human diseases. In the present studies, the radical was generated by exposure of hydrogen peroxide to 254 nm light in the presence of native calf thymus DNA. Single strand breaks, decrease in Tm and modification of adenine and thymine were some of the modifications observed in nDNA. Antibodies induced in experimental animals against the modified DNA were immunogen specific. These antibodies also recognize native B-conformation. It was observed that naturally occurring anti-native DNA autoantibodies from SLE sera recognize modified DNA in direct binding and competition ELISA. Gel retardation assay reiterated the formation of immune complexes between induced antibodies and DNA fragments of around 300 bp (B-conformation). The possible significance of these findings in the etiology of SLE has been discussed.
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PMID:Antibodies against free radical modified native DNA recognize B-conformation. 133 Sep 2

DNA samples from control and lupus lymphocytes were studied for DNA integrity and single-strand breaks by agarose gel electrophoresis following digestion with the enzyme S1 nuclease. S1 nuclease digests single-strand gaps in double-stranded DNA. Gel patterns of phytohemagglutinin (PHA)-stimulated control and lupus lymphocyte DNAs were identical in the absence of S1 nuclease incubation. DNA isolated from PHA-stimulated control lymphocytes was relatively resistant to S1 nuclease digestion in 14 of 16 samples. However, 15 of 16 DNA samples from PHA-stimulated lupus lymphocytes demonstrated dramatically greater S1 nuclease digestion than paired control DNAs from lymphocytes analyzed at the same time under the same conditions. Increased S1 sensitivity suggests that more single-strand DNA breaks were found in PHA-stimulated lupus lymphocytes and/or the lupus DNA was more damaged than control DNA. We suggest that structural changes found in DNA from stimulated T lymphocytes of lupus patients are consistent with an endogenous antigen-mediated disorder.
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PMID:Phytohemagglutinin-stimulated lymphocytes from patients with systemic lupus erythematosus demonstrate DNA damage. 194 28

Antigen DNA isolated from immune complexes present in plasma of three patients with active systemic lupus erythematosus using an affinity column was cloned and sequenced. One clone, designated pKS7, was found to have a region homologous with that of the E. coli metK gene, and another, designated pKS8, had a region homologous with a sequence including the replication origin of bacteriophage f1. Gel retardation assay revealed that pKS7 and pKS8 interacted with the patient's IgG fraction to form immune complexes, respectively. The affinity-purified antigen DNA was proved to be originated from bacteria or bacteriophage.
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PMID:Demonstration of extrinsic DNA from immune complexes in plasma of a patient with systemic lupus erythematosus. 198 12

We have identified an inhibitor of the protein C anticoagulant pathway in the plasma of a patient with systemic lupus erythematosus and a history of recurrent deep vein thrombosis, fetal wastage, and seizures. The patient's plasma contained anticardiolipin antibodies as well as a weak lupus anticoagulant. Examination of this patient's plasma revealed normal levels of protein C and protein S antigen, normal levels of functional protein C, as well as essentially normal levels of every blood coagulation factor. In a modified prothrombin time assay, the activated protein C-mediated prolongation of the clotting time observed in normal plasma was not observed in this patient's plasma. Gel permeation chromatography of the patient's plasma revealed that the inhibitory material was a high molecular weight protein that coeluted with the IgM peak. The inhibitor did not appear to circulate as a complex with protein C, since the inhibitor could easily be separated from protein C during fractionation procedures, and did not interfere with the activation of protein C in plasma as assessed by a functional amidolytic assay. Our findings suggest that the recurrent thrombotic episodes observed in this patient may have occurred as a result of the patient's antiphospholipid antibody neutralizing specific phospholipids essential for the full expression of the anticoagulant activity of activated protein C.
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PMID:Impairment of the protein C anticoagulant pathway in a patient with systemic lupus erythematosus, anticardiolipin antibodies and thrombosis. 210 91

An anti-C1q capture method kit (C1q-immunoglobulin G [IgG]) (Ortho Diagnostics, Inc., Raritan, N.J.) for measuring circulating immune complexes (CIC) was evaluated. The kit showed poor diagnostic sensitivity (P less than 0.005) for identifying CIC in patients with systemic lupus, rheumatoid arthritis, and bacterial endocarditis, as compared with polyethylene glycol-IgG and Raji cell tests (12, 24, and 24 positive, respectively, of 31 patients). Of the patients who were positive with the C1q-IgG test, 25% showed discrepancies when their results were compared with the polyethylene glycol-IgG and C1q-binding test results. Gel filtration chromatography of two of these discrepant sera showed the only peak of C1q-IgG activity to be associated with monomeric IgG (molecular weight, less than 200,000). We concluded that the kit method may be measuring substances other than CIC in some sera, because molecules of C1q attached to IgG should exhibit a molecular weight of greater than 500,000.
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PMID:Evaluation of anti-C1q capture assay for detecting circulating immune complexes and comparison with polyethylene glycol-immunoglobulin G, C1q-binding, and Raji cell methods. 295 87

A sensitive enzyme immunoassay was developed for the determination of urokinase in the plasma and urine. Normal human urine contained 2.68 +/- 0.36 u/ml of UK. Gel filtration of the mixture of normal urine resulted in 2 peaks in the profile, one with molecular weight of 32,000 and the other with molecular weight of 22,000. Patients with glomerulonephritis had higher UK levels. Kidneys with minimal changes and mild type or with the inactive phase of systemic lupus erythematosus (SLE) secreted relatively high levels of UK in the urine.
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PMID:Determination of urokinase in the urine of healthy volunteers and patients with renal diseases. 354 Dec 83

The effect of the sera of patients with systemic lupus erythematosus (SLE) on monocyte function was studied using cell spreading as an indicator. Monocyte spreading induced by exogenous stimuli was shown to be inhibited by SLE sera. Gel filtration of SLE sera on Sephadex G-200 revealed that the factor responsible for this inhibition had a molecular weight of about 50,000. Pretreatment of monocytes with the inhibitory factor led to suppression of cell spreading induced by subsequent stimulation, but this hyporeactivity was reversible. Spreading of monocytes was rapidly aborted by the addition of this inhibitory factor. Thus, the inhibitory factor appeared to affect monocyte itself, but its effect seemed to be transient.
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PMID:An inhibitory factor against monocyte spreading in the sera of patients with systemic lupus erythematosus. 389 23

The present authors and Olds et al. reported that the anti-F(ab')2 antibodies (Abs) in serum interfere with the solid phase (SP) anti-C3 immune complex assay. The anti-F(ab')2 Abs in human sera bind solid phase F(ab')2 anti-C3 of rabbit or goat, and were measured erroneously as C3 bearing circulating immune complexes (CIC). Gel filtration analysis of SP anti-C3 assay revealed that C3 bearing CIC is detected only in heavy fractions and 7S CIC-like activity is not CIC but anti-F(ab')2 activity. As the molecular weight of such CIC is heavy enough to be precipitated by 5% polyethylene glycol (PEG) and IgG anti-F(ab')2 Abs and free C3 are not included in 5% PEG precipitates, 5% PEG precipitates of the test sera were used for SP anti-C3 (Modified SP anti-C3). CIC measured by modified SP anti-C3 were positive in 14/16 at active stage of SLE and positive only in 2/16 at inactive stage. CIC by this test were also correlated well to serum complement activity, and were thought to be clinically reliable and useful.
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PMID:Modified anti-C3 immune complex assay which avoids interference by anti-F(ab')2 antibodies. 393 Dec 96


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