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 lupus-like syndrome involving chronic urticaria with cutaneous vasculitis, systemic symptoms, hypocomplementemia with preferential depletion of C1q, and low m.w. (7S) C1q-precipitins has recently been defined. The C1q-precipitin activity (C1q-p) seems to represent a diagnostic marker of the disease, but its chemical nature is not yet clear. We have partially purified and characterized C1q-p from the serum of two patients with this syndrome and compared its activity with the C1q-precipitating activity of aggregated human gamma-globulin (AHGG) anti-C1q antibodies, and several polynucleotides including DNA and polyinosinic acid. C1q-p was found to partition with IgG during precipitation by ammonium sulfate and low ionic strength buffer as well as during column chromatography on DEAE-cellulose and G-200 Sephadex. Like AHGG, but in complete contrast to the polynucleotides, the C1q-precipitating activity of C1q-p was sensitive to pepsin, trypsin, and acidic conditions, but unaffected by DNAse or RNAse; the C1q-precipitating activity of anti-C1q antibody was not diminished by any of these procedures. Thus, C1q-p consists of gamma-migrating protein of low m.w., and its C1q-precipitating activity is indistinguishable from that of AHGG. These results are consistent with the concept that C1q-p is comprised, at least in part, of IgG that binds C1q via the Fc portion of the molecule.
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PMID:Low molecular weight C1q-precipitins in hypocomplementemic vasculitis-urticaria syndrome: partial purification and characterization as immunoglobulin. 2 69

Antilymphocyte antibodies in normal and SLE sera were found to react with lymphocytes fixed in acetone at -30 degrees C. for 10 minutes. At a dilution of 1:40, 3.7 per cent of normal and 90.9 per cent of SLE sera were positive with the use of indirect immunofluorescence with a pepsin-digested, FITC-labeled anti-Fab serum. The reaction was independent of temperature between 4 degrees and 37 degrees C. Three patterns of staining were seen in the lymphocyte surface: reticular, ring, and globular. The ring pattern appeared to correlate with IgM, and the reticular and globular patterns with IgG antilymphocyte antibodies. Absorption with lymphocytes, insolubilized extracts of rat liver and kidney, and human brain revealed that antilymphocyte and ANA activity could be independently removed. Variation in reactivity with cells from different normal donors was similar to that seen with the microcytotoxicity test. Acetone-fixed lymphocytes appear to be a much more sensitive target than viable cells in suspencion in IIF tests for antilymphocyte antibodies. The IIF test with fixed cells also appears slightly more sensitive than cytotoxicity testing and has the advantage of allowing storage of target cells.
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PMID:Detection of antilymphocyte antibodies in patients with systemic lupus erythematosus by indirect immunofluorescence on acetone-fixed lymphocytes. 31 79

Purified anti-dsDNA antibody was obtained from the serum of patients with systemic lupus erythematosus by affinity-column chromatography. Anti-dsDNA-F(ab')2 fragment (idiotype) was prepared from digested anti-dsDNA antibody with pepsin. We have developed a sensitive and specific method for detection anti-dsDNA-F(ab')2 antibody. Our result revealed that low titer of anti-dsDNA was observed in patients with active stage of systemic lupus erythematosus.
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PMID:[Detection of anti-dsDNA-F(AB')2 antibody and evaluation of its clinical significance]. 128 85

In earlier studies we showed that the C1q-binding IgG in the sera from patients with systemic lupus erythematosus (SLE) tested by C1q solid-phase radioimmunoassay is cofractionated with monomeric IgG on gel filtration and mostly binds to C1q via the F(ab')2 region. In this study, we found that C1q, even when stripped of its immune complex-binding globular regions by pepsin digestion, retained a substantial part of its ability to bind IgG from SLE sera, suggesting that the collagen-like region of C1q is involved in binding to the SLE IgG. Heat-inactivation of C1q also failed to abolish its ability to bind IgG from SLE sera. In contrast, the binding of C1q to heat-aggregated IgG was completely abrogated by these treatments. In addition, the reaction of heat-aggregated IgG with the solid-phase C1q was markedly dependent on ionic strength whereas the binding of IgG from SLE sera with the solid-phase C1q persisted at high concentrations of salt. These findings suggest that the Clq-binding IgG in SLE sera is, at least in part, antibody directed against the collagen-like region of C1q.
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PMID:C1q solid-phase radioimmunoassay: evidence for detection of antibody directed against the collagen-like region of C1q in sera from patients with systemic lupus erythematosus. 349 89

A micro-enzyme linked immunosorbent assay (ELISA) aimed at detecting anti-fibronectin (anti-Fn) antibodies has been developed and standardized. Fifty sera from systemic lupus erythematosus (SLE), 50 from rheumatoid arthritis (RA) patients, as well as 200 sera from patients with bacterial or viral infections were assayed for the presence of anti-Fn autoantibodies. The IgG fractions of three representative positive sera (1 SLE, 1 RA and 1 streptococcal endocarditis) were digested with pepsin and the resulting F(ab')2 fragment assayed in the test. The presence of the anti-Fn activity in these fragments as well as lack of correlation in individual sera between the level of anti-Fn (as determined by ELISA) and that of Ig or immune complexes, suggest that our anti-Fn autoantibodies are indeed detected in our assay. The meaning of these antibodies, which were also found with bacterial and viral infections is discussed within the frame of the fibronectin biological properties.
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PMID:[Anti-fibronectin autoantibodies in systemic lupus erythematosus, rheumatoid polyarthritis, and various viral or bacterial infectious diseases]. 351 85

Anti-endothelial cell antibodies (AECA) have been detected in autoimmune diseases such as systemic lupus erythematosus (SLE) and scleroderma (PSS) but their role in pathogenesis is unknown. Immunofluorescence, immunohistochemistry, complement-dependent antibody lysis, and radioimmunoassay have been used in the past to detect AECA. We have developed a rapid, sensitive, and quantitative cellular enzyme-linked immunosorbent assay (ELISA) to detect and characterize AECA. Sera were obtained from 28 normal volunteers, 28 patients with SLE, and 14 patients with PSS. We also performed studies in 47 patients with various monoclonal gammopathies. Endothelial cells (EC) were obtained from human umbilical veins by standard methods and subcultured on 96-well tissue culture plates without fixation. EC were then sequentially incubated with sera, peroxidase-conjugated goat anti-human Ig (IgG, IgM, or IgA), and substrate. Optical density readings were converted to arbitrary units by developing a standard curve. Heavy-chain specific antibodies were used to determine the class of AECA binding to EC. IgG was purified by using protein A columns and digested with pepsin to obtain F(ab')2 fragments. The mean units of AECA from normals were 19.3 for IgG and 12.5 for IgM. SLE sera showed significant levels of IgM AECA (37 units, P less than 0.001) but not IgG (29 units, P less than 0.1). PSS sera showed significant levels of both IgM AECA (38 units, P = 0.001) and IgG AECA (42.7 units, P less than 0.005). IgA AECA were not detected in normal, SLE, or PSS sera. Blocking Fc receptors with rabbit IgG did not affect the titer of IgG or IgM AECA.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Anti-endothelial cell antibodies: detection and characterization using a cellular enzyme-linked immunosorbent assay. 354 64

Components were solubilized from human glomerular basement membrane by digestion with collagenase and pepsin or by extraction with guanidine-HCl either directly or after previous digestion with the enzyme. The diverse preparations were used as antigens in the enzyme-linked immunosorbent assay (ELISA) of antibody titers in sera from patients with Goodpasture syndrome and patients with other forms of glomerulonephritis, that is, systemic lupus erythematosus, periarteritis nodosa, and IgA-related nephropathy. Patients with Goodpasture syndrome had high titers of IgG antibodies reacting most strongly with collagenase digests. The antigen(s) was only partly solubilized by guanidine-HCl extraction, was destroyed by pepsin digestion as well as reduction, and partly destroyed by trypsin digestion. The antigen(s) is most likely noncollagenous protein. Antibodies from patients with other forms of nephritis were directed primarily against antigens in guanidine-HCl extracts, while the antigen(s) was not solubilized by collagenase digestion. Pepsin digestion destroyed the antigen(s). The antibodies were of a different class, that is, the patients with systemic lupus erythematosus had IgG and IgA as well as IgM antibodies; the patients with periarteritis nodosa had IgM or IgG and IgA antibodies, while the patients with IgA-related nephritis had the highest recorded titers of IgA but also had IgG as well as IgM antibodies. None of the patients had antibodies directed against triple helical collagen. The antibody response in anti-GBM antibody-related nephritis, then, is different both with respect to antigen and antibody class and depends on the underlying disease syndrome.
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PMID:Antiglomerular basement membrane antibody: antibody specificity in different forms of glomerulonephritis. 613 25

Rabbit antisera were produced against pooled living lymphocytes from 25 patients with active systemic lupus erythematosus (SLE). Lymphocytes collected at plasmapheresis or venipuncture were frozen in liquid nitrogen and later coated with rabbit antibody to normal human tonsils and normal thymocytes immediately before intravenous immunization of rabbits. Antisera were subsequently extensively absorbed with normal human tonsillar cells, thymocytes, peripheral blood lymphocytes, erythrocytes, and leukocytes from patients with myelogeneous and lymphatic leukemia until residual base-line immunofluorescent staining of normal human lymphocytes using F(ab)2' of whole antisera averaged less than 5%. Absorbed pepsin-digested antisera detected membrane antigens which were markedly increased (mean 32%) on lymphocytes from patients with active SLE (P less than 0.05). Membrane antigens reacting with absorbed, pepsin-digested antisera were present on both T and B cells but, in most instances, predominated on T cells. Control observations using absorbed pepsin-digested antisera to normal human lymphocytes or peripheral blood lymphocytes from patients with rheumatoid arthritis showed no similar specificity. SLE patients treated with moderate or high dose corticosteroids or immunosuppressive agents (cytoxan or azathioprine) appeared to lose lymphocyte antigens detected by these reagents. Control studies with other connective tissue disease patients, miscellaneous hospitalized subjects, or normal controls showed low levels of reactivity (2-5%). SLE lymphocyte membrane antigens uniquely increased during active disease; this may represent neoantigens or alterations associated with the disease itself.
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PMID:Lymphocyte antigens in systemic lupus erythematosus: studies with heterologous antisera. 615 83

A technique is described which allows the antibodies of circulating immune complexes to be isolated as their F(ab')2 fragments. The method is based on the precipitation of the complexes by the sequential addition of conglutinin and anti-conglutinin, and the subsequent digestion of these precipitates by pepsin. Using this technique it has been possible to show antibodies to Epstein-Barr (EB) virus antigens in the immune complexes of patients with Burkitt's lymphoma and to microbial antigens in two patients with nephritis. By substituting DNAase for pepsin it has also been possible to show antibodies to DNA-containing nuclear antigens in the serum of patients with systemic lupus erythematosus.
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PMID:The isolation of the antibody moieties of immune complexes from serum by the pepsin digestion of conglutinin-anti-conglutinin complexes. 627 42

The molecular size of C1q-binding immunoglobulin (Ig) G complexes in systemic lupus erythematosus (SLE) sera was studied by gel filtration using C1q solid-phase radioimmunoassay (C1q SPRIA). All 15 SLE sera tested contained predominantly small-sized IgG complexes, cofractionating with monomeric IgG. In contrast to heat-aggregated IgG, these small-sized IgG complexes retained C1q-binding activity even after pepsin digestion, exposure to low pH, or reduction and alkylation, suggesting that the F(ab')2 region is involved in C1q-binding activity of these complexes. To see whether anti-C1q antibodies or small antigen-IgG complexes, which bind to C1q via their antigens, are responsible for C1q-binding activity via the F(ab')2 region, the pepsin-digested Ig fractions of SLE sera were fractionated at high salt. C1q-binding activity in the fractions corresponding to the F(ab')2 region increased 2.5- to 3.9-fold at high salt. These results suggest that the C1q-binding, small-sized IgG complexes may be comprised mostly of anti-C1q antibodies and that some of the antibodies, which are dissociated with their antigens at high salt, might be cross-reactive with C1q.
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PMID:Characterization of C1q-binding IgG complexes in systemic lupus erythematosus. 642 20


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