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 phenanthridine dye ethidium bromide (EB) intercalates with double-stranded DNA (dsDNA) resulting in an enhancement of fluorescence. Single-stranded DNA (ssDNA) does not show this fluorescent enhancement. Purified IgG from patients with Systemic Lupus Erythematosus (SLE) containing anti-dsDNA antibodies competes with EB for binding to DNA resulting in a decrease in fluorescence. This study has shown that antibodies which bind ssDNA in the Millipore filter radioimmunoassay displace EB from dsDNA showing that antigenic determinants are available for binding in the double-stranded molecule. This study introduces the EB assay and presents a comparison with the Millipore filter assay.
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PMID:The binding of anti-DNA antibodies as measured fluorometrically by ethidium bromide. 8 77

The two-color method originally described by Van Rood et al. (Van Rood, J. J., A. Van Leeuwen, and J. S. Ploen. 1976. Simultaneous detection of two cell populations by two-color fluorescence and application to the recognition of B-cell determinants. Nature (Lond.). 262: 795-797) for the typing of homologous leukocytic antibodies, D-region was used for the detection of antilymphocyte antibody (ALA) in systemic lupus erythematosus. In this method, surface immunoglobulin-bearing cells were identified with fluorescein isothiocyanate-labeled anti-immunoglobulin and nuclei of killed cells were stained with ethidium bromide. Therefore, cell type (T or B) of the target cells can be identified without fractionating them. ALA was detected in 87% of lupus sera and had a preferential reactivity with T cells. Its major immunoglobulin class was shown to be immunoglobulin (Ig)M. The subspecificity of ALA was further analyzed using fractionated T-cell subsets as target cells. When T lymphocytes were separated into Fc receptor-bearing (Tgamma) and lacking (Tgamma[-]) cells, 64% of ALA showed preferential reactivity with Tgamma cells and 14% with Tgamma(-) cells. The remainder had no selective reactivity against Tgamma or Tgamma(-) cells. Tgamma cells were shown to have suppressor activity, whereas Tgamma(-) cells were indicated to contain helper cells. The above finding was in agreement with the observation that treatment of T cells with ALA that preferentially react with Tgamma cells considerably enhanced immunoglobulin synthesis in vitro, whereas treatment of T cells with ALA reactive with Tgamma(-) cells clearly suppressed the formation of immunoglobulins. Treatment of ALA with no selective reactivity showed variable effects on in vitro immunoglobulin synthesis. These results indicate that ALA in lupus have heterogeneous specificities against human T-cell subsets.
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PMID:Detection of antilymphocyte antibody with two-color method in systemic lupus erythematosus and its heterogeneous specificities against human T-cell subsets. 9 23

A method for obtaining luminescent sera, consisting in isolation of pure antigens G, A, M from human gamma-globulin and blood serum from patients with myeloma disease is suggested. A native antiserum was obtained by immunization of rabbits with water-insoluble polycondensate of antigens "sewn" with glutaric aldehyde. Adsorption of antisera as well as specific antigens was carried out with antigen- and antibodyimmunosorbent, the latter being obtained with the help of both glutaric aldehyde and sefarose 4B treated with cyanogen bromide. The sera had a specific titre in the precipitation reaction against their own antigens 1:32 and were highly specific. A globulin fraction was obtained by sedimentation with polyethylene-glycol. Marking of the specific protein with fluoresceine isothiocyanate was carried out using the dialysis method with subsequent purification on sefadex and DEAE-cellulose. The application of the abovementioned sera made it possible to ascertain the character of distribution of deposits of immunoglobulins in glomeruli in systemic lupus erythematodes, glomerulonephritis and in the cells of the synovial fluid sediment in rhematoid arthritis.
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PMID:[Utilization of luminescent monospecific sera against human immunoglobulins G, A and M for diagnostic purposes]. 110 50

Autoantibodies directed at the intracellular Ro ribonucleoprotein complex are found in the serum of patients with systemic lupus erythematosus (SLE) and related autoimmune diseases. The antigenic stimulus for the induction of these autoantibodies is unknown, although we have previously demonstrated that the Ro protein and immunoglobulin G (IgG) share immunologic determinants bound by anti-Ro antibodies. The present study further defines the fine specificity of this cross-reactive binding. Using both patient autoanti-Ro antibodies and antigen-induced rabbit anti-Ro serum, the binding specificity for IgG was located to the heavy chains of IgG outside the Fc domain. F(ab')2 fragments of IgG were observed to inhibit specific Ro binding by either human or antigen-induced rabbit sera, while Fc fragments of IgG failed to inhibit Ro binding. Anti-Ro sera were found to bind the heavy chains of IgG in immunoblots, and the antibodies eluted from these heavy chains were capable of immunoprecipitating the Ro particle from human cell extracts. Not all patient sera with anti-Ro antibodies possessed IgG binding antibodies. Studies of cyanogen bromide digestion fragments of IgG implicate the hinge region of IgG as the region cross-reactive with the Ro protein. The nature of this cross-reactivity may be important in understanding the induction and/or perpetuation of the anti-Ro response in patients with autoimmune disease.
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PMID:Anti-Ro autoantibody with cross-reactive binding to the heavy chain of immunoglobulin G. 129 Feb 72

Antibodies to human type II collagen were examined in the sera of 105 patients with rheumatoid arthritis (RA), 44 patients with systemic lupus erythematosus (SLE) and 11 patients who fulfilled the criteria of both diseases (RA-SLE overlap), using a solid-phase radioimmunoassay (RIA). The frequencies of antibodies to native and denatured human type II collagen were 20% and 27% in RA, 14% and 16% in SLE, and 45% and 36% in RA-SLE overlap. The specificity of the antibodies was further examined by inhibition with native and denatured type II collagen, by immunoblotting on native and denatured type II collagen, and by immunoblotting on cyanogen-bromide derived polypeptides of type II collagen. We could not identify any disease-specific patterns of reactivity. Thus, in the three disease groups the antibody response was polyclonal; there were antibody populations that reacted with native and/or denatured collagen, and epitopes could be assigned to at least three CB peptides, CB10.5, CB11 and CB8.
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PMID:Epitope specificity of antibodies to type II collagen in rheumatoid arthritis and systemic lupus erythematosus. 138 2

The role of autoimmunity to type II collagen in the arthritis of systemic lupus erythematosus (SLE) has been assessed by ELISA and by Western blotting cyanogen bromide cleavage fragments separated on SDS-PAGE. The results show that antibodies to both native and heat-denatured collagen are quite common in SLE when measured by ELISA. Of particular interest is the demonstration of an association between antibodies to the CB 11 peptide and deforming arthritis in SLE. This is the arthritogenic peptide in murine models of collagen II-induced autoimmune arthritis and the results presented here suggest a potential pathogenetic role in the deforming arthritis of SLE for this specific subset of antibodies to type II collagen.
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PMID:Antibodies to type II collagen in SLE: a role in the pathogenesis of deforming arthritis? 169 Jun 83

The role of interleukin-4 (IL-4) and interferon-gamma (IFN-gamma) in the pathogenesis of the collagen vascular diseases was studied. The serum level of IL-4 was decreased in patients with systemic lupus erythematosus (SLE) and mixed connective tissue disease (MCTD), and was variable in patients with rheumatoid arthritis (RA). The serum level of IFN-gamma was increased in patients with SLE, MCTD and RA. In patients with SLE, there was an inverse correlation between the levels of IL-4 and IFN-gamma. The proliferation and immunoglobulin production of the high-density-B cells in response to IL-4 was suppressed in normal controls, although the degree of suppression was less in patients with SLE. Cell cycle analysis using ethidium bromide demonstrated the similar findings. These data suggest that IL-4 and IFN-gamma might participate in regulating both of growth and differentiation of B cells in vivo. However, immunoglobulin production by whole B cells in response to IL-2 or PHA-induced T-cell factor was extensively facilitated by IFN-gamma in patients with SLE. It is possible that IFN-gamma enhances the differentiation of already-activated B cells, and that polyclonal B cell activation is promoted. Therefore, the failure of the regulatory mechanism by these cytokines might be related to the pathogenesis of these diseases.
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PMID:[Relationship between serum interleukin-4 or interferon-gamma level and B cell abnormality in patients with collagen vascular diseases]. 176 43

Plasmapheresis fluids from 20 patients with clinically active SLE, from three patients with Waldenstrom's disease, from three patients with rheumatoid arthritis, two patients with myasthenia gravis and other diseases including active systemic disorders were precipitated using polyethylene glycol 6000 (PEG). By applying ethidium bromide staining, plasma nucleic acids (PNA) could be demonstrated in PEG-precipitates of SLE patients exclusively. Purified immunoglobulins of SLE plasma precipitates were shown to form antigen-antibody complexes with PNA as demonstrated by electronmicroscopy. Further characterization of PNA by agarose gel electrophoresis revealed a molecular weight up to 20 kbp. Cesium chloride buoyant density gradients showed non-homogeneous molecules, excluding pure microbial origin. In spite of RNase digestion, the PNA contained RNA with 30-70% riboguanosine as shown by nucleoside analysis. The high amount of guanosine-rich RNA was further supported by similarities between PNA and polyriboguanylic acid in hyperchrome shifting due to thermic denaturation. HPLC analysis showed a molecular weight of ribonucleic acids of more than 60 b thus excluding mere oligonucleotides. In contrast to B-type dsDNA, PNA from SLE patients were immunogenic. Antibodies against PNA could be induced in rabbits by subcutaneous injection. The antisera thus obtained showed crossreactivity with polyriboguanylic acid and dsDNA preparations.
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PMID:Antibody binding of macromolecular DNA and RNA in the plasma of SLE patients. 246 74

RNA molecules immunoprecipitated with sera from patients who have rheumatic diseases can be readily detected in polyacrylamide gels by using ethidium bromide and silver stains. With these stains, we found that RNA patterns characteristic of a broad range of specific small nuclear ribonucleoproteins and small cytoplasmic ribonucleoproteins were recognizable. The stains correctly identified antibodies to ribonucleoproteins in 33 (92%) of 36 patient sera selected for study because of known antibody specificities. The silver stain method detected antibodies to ribonucleoproteins in 25 (76%) of 33 patients with classic systemic lupus erythematosus, a frequency that approximated the frequency observed in the Lerner-Steitz assay, which is based on autoradiography. This approach considerably simplifies the latter radioimmunoassay with minimal loss of precision and sensitivity.
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PMID:Detection of antibodies to small nuclear ribonucleoproteins and small cytoplasmic ribonucleoproteins using unlabeled cell extracts. 293 57

An immunoadsorbent based on immobilized C1q has been developed to remove possibly pathogenic immune complexes from plasma deriving from patients suffering from systemic lupus erythematosus or rheumatoid arthritis. Traditional immobilization procedures based on, e.g., cyanogen bromide activation could not be used to produce an efficient adsorbent. However, by using antibodies directed towards C1q as handles for the immobilization of C1q it was possible to make an adsorbent that efficiently bound immune complexes in plasma. The capacity of the C1q anti-C1q adsorbent to bind artificial immune complexes such as aggregated human globulins or immune complexes from various plasma samples was evaluated. Both batch and column experiments were conducted. The typical capacity in batch was about 1 mg immune complexes/ml gel when incubated with patient plasma samples with high titers of immune complexes. Special attention has to be paid to leakage of undesirable components from the adsorbent. It was found that leakage of C1q occurred but it was not more than after covalent immobilization procedures such as cyanogen bromide.
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PMID:The development of a C1q anti-C1q immunoadsorbent for removal of immune complexes from plasma. 326 46


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