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)

Indirect immunofluorescence revealed the presence of pemphigus-like antigenic activity on SCaBER cell monolayers after incubation with sera from patients with pemphigus vulgaris. In contrast, no fluorescence was observed after incubation of the cells with sera from patients with bullous pemphigoid, systemic lupus erythematosus or healthy individuals. In order to identify this pemphigus-like antigen, the SCaBER cell membrane proteins were solubilized in non-ionic detergent, separated according to their molecular weight by sodium dodecyl sulphate polyacrylamide gel electrophoresis (SDS-PAGE) and electrophoretically transferred to nitrocellulose sheets. After incubation with pemphigus serum followed by 125I-radiolabelled goat anti-human IgG, autoradiography revealed pemphigus antibody binding activity in the 105 Kd region in electrophoretograms of the unreduced SCaBER cell membrane extracts. This pemphigus-like antigen was isolated by affinity chromatography on the Sepharose-linked IgG fraction of sera from patients with pemphigus vulgaris.
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PMID:Identification of pemphigus-like antigens expressed by SCaBER cells. 388 26

Ribonucleoprotein particles containing Sm antigen were separated from particles containing both Sm and RNP antigens by ion-exchange chromatography to study the recognition of these antigens by autoimmune sera. By using the separated antigens, anti-Sm and/or anti-RNP antibodies were detected in approximately 60% of sera from systemic lupus erythematosus patients by both enzyme-linked immunosorbent assay and immunoprecipitation of radiolabeled antigens followed by analysis on sodium dodecyl sulfate-polyacrylamide gels. These antibodies were detected in 30% of the same sera using the standard passive hemagglutination technique. Competition experiments demonstrated that all of the sera tested that contained anti-Sm antibodies also had anti-RNP-like reactivity. This latter reactivity usually represented 80% or more of the total Sm and RNP binding activity in lupus sera. The binding to RNP-like determinants by several of the sera was uniquely resistant to treatment of the antigen with snake venom exonuclease. These studies indicate that humoral immunity against Sm and RNP antigens in systemic lupus erythematosus is directed primarily against a single type of ribonucleoprotein particle in which the two antigens are physically associated. The specific binding to a single type of ribonucleoprotein particle suggests that this particle may be especially immunogenic and that it might play an important role in induction of the humoral immune response to Sm and RNP.
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PMID:Autoimmune sera reactive with Sm antigen contain high levels of RNP-like antibodies. 397 19

A 20-year-old patient had systemic lupus erythematosus and extensive generalized discoid disease that failed to respond to conventional treatment with topical steroids and high doses of hydroxychloroquine sulfate (Plaquenil). The skin lesions responded dramatically to 100 mg of azathioprine sodium daily, flared when the drug treatment was discontinued, and again responded on reinstatement of the same dosage of azathioprine. The case report suggests that extensive discoid skin lesions can be successfully treated with oral azathioprine.
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PMID:Successful treatment of generalized discoid skin lesions with azathioprine. Its use in a patient with systemic lupus erythematosus. 403 29

Surface radioiodination of lymphocytes by the lactoperoxidase procedure has permitted demonstration of an assortment of different antibodies to lymphocytes in the sera of patients with systemic lupus erythematosus. One type of antibody proved of special interest because it appeared to be associated with inhibition of the responder cells in the mixed leukocyte culture reactions. This reacted with an antigen on T cells and thymocytes which on sodium dodecyl sulfate acrylamide gel electrophoresis showed a molecular weight of approximately 15,000 daltons. The possible relation of this antigen to T cell receptors and products of immune response genes is discussed.
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PMID:Antibodies to a specific surface antigen of T cells in human sera inhibiting mixed leukocyte culture reactions. 454 34

The activity of phospholipase inhibitory protein, lipomodulin, partially purified from rabbit neutrophils, was markedly decreased after treatment with sera from patients with rheumatic diseases such as systemic lupus erythematosus, rheumatoid arthritis, and dermatomyositis. The decrease of the protein's inhibitory activity on phospholipase A2 paralleled the amount of [35S]methionine-labeled lipomodulin precipitated by the sera. Absorption of patients' sera with anti-human IgM (mu chain) or protein A-agarose, but not with anti-human IgG (gamma chain), decreased their ability to decrease the activity of lipomodulin on phospholipase A2 or to precipitate the radioactive lipomodulin. The IgM fraction of patients' sera could precipitate [35S]methionine-labeled lipomodulin (40,000 daltons) which comigrated with highly purified lipomodulin on gel electrophoresis with sodium dodecyl sulfate. All of these observations suggest that the sera of many patients with rheumatic diseases contain autoantibody against lipomodulin. A monoclonal antibody against lipomodulin was also obtained. Stimulating human fibroblasts with bradykinin in the presence of monoclonal antilipomodulin antibody markedly enhanced arachidonic acid release due to the activation of phospholipase(s) in the intact cells, and this stimulatory effect was blocked by adding purified lipomodulin. These findings suggest that lipomodulin regulates the activity of phospholipase(s) on the cell surface and that autoantibodies against lipomodulin may play a role in certain symptoms of rheumatic diseases, especially by the formation of prostaglandins and other metabolites of arachidonic acid.
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PMID:Presence of autoantibody for phospholipase inhibitory protein, lipomodulin, in patients with rheumatic diseases. 611 91

Sera from majority of patients with seropositive rheumatoid arthritis, which generally lacked detectable anti-double stranded DNA in Farr, Crithidia luciliae, and microcomplement fixation assays, exhibited high levels of dsDNA binding in the presence of 3.5% polyethylene glycol when using intrinsically labeled 3H-PM2 DNA as antigen. Except for SLE, such increased dsDNA binding was absent in normal and a variety of other disease sera, including those from patients with seronegative rheumatoid arthritis. In contrast to the situation in SLE, in which dsDNA binding is mediated by specific anti-DNA antibody, the increased dsDNA binding activity in seropositive rheumatoid arthritis was shown to be dependent upon complex low avidity interactions involving DNA, IgG, IgM rheumatoid factor, and low density lipoproteins. Analysis of the composition of the polyethylene glycol serum precipitates by 2-dimensional gel diffusion, immunoelectrophoresis, and sodium dodecyl sulfate polyacrylamide gel electrophoresis failed to reveal the presence of additional DNA-binding proteins unique to seropositive rheumatoid arthritis. The only feature distinguishing high DNA binding sera from those with low DNA binding activity was an increased amount of polyethylene glycol-insoluble IgG in the former, presumably reflecting IgG/IgG and/or IgG/IgM complexes. The significance of these unusual DNA/low density lipoprotein/IgG/rheumatoid factor complexes with respect to the diagnostic specificity and pathophysiology of the DNA/anti-DNA system is discussed.
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PMID:Nature of double-stranded DNA binding activity in seropositive rheumatoid arthritis: formation of low avidity DNA/rheumatoid factor/IgG/low density lipoprotein complexes. 616 94

Purified serum antibodies of patients suffering from mixed connective tissue disease were tested for their immunological specificity against nuclear constituents of HeLa S3 cells. In the indirect immunofluorescent staining technique, using cells and nuclei as targets, a typical speckled intranuclear staining pattern was obtained, that persisted after degradation and extraction of all nucleic acids and their associated proteins. This treatment of nuclei with detergents, DNase, RNase and high salt concentrations leave intact only the so-called nuclear matrix which is an intranuclear proteinaceous network. Further proof that nuclear matrix proteins were targets of the autoimmune reaction was obtained after separation of these proteins by sodium dodecyl sulfate polyacrylamide gel electrophoresis and electrophoretic transfer to nitrocellulose (blotting). A specific number of blot-transferred matrix proteins reacted with purified serum antibodies of 10 patients with mixed connective tissue disease, whereas this reaction was negative with normal healthy individuals. IgG preparations of 7 patients with systemic lupus erythematosus showed a weak, if any, reaction with matrix constituents. Obviously, in some connective tissue diseases serum antibodies are expressed which are directed to specific nuclear matrix antigens.
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PMID:Anti-nuclear matrix antibodies in mixed connective tissue disease. 618 28

Lipomodulin, purified to near homogeneity from rabbit peritoneal neutrophils, was phosphorylated by cyclic AMP-dependent protein kinase from bovine heart with concomitant loss of its ability to inhibit phospholipase A2 from porcine pancreas. Phosphorylation of lipomodulin was confirmed by the incorporation of 32P from [gamma-32P]ATP. To demonstrate that lipomodulin undergoes phosphorylation in vivo, rabbit peritoneal neutrophils were incubated with 32P and lipomoculin was isolated by immunoprecipitation with serum from a patient with systemic lupus erythematosus which has anti-lipomodulin antibody. Analysis of 32P-labeled immunoprecipitates by sodium dodecyl sulfate electrophoresis revealed a single peak of radioactivity that comigrated with [35S]methionine-labeled lipomodulin. The administration of a chemoattractant, N-formyl-methionyl-leucyl-phenylalanine to intact rabbit neutrophils, resulted in a marked increase in arachidonate release from the cells and an increase in 32P incorporation into lipomodulin. A close correlation was found between the extent of phosphorylation of lipomodulin and the rate of arachidonate release. Phosphorylation of lipomodulin in neutrophils gradually returned to the control level with corresponding cessation of arachidonate release. In contrast to the in vitro system, phosphorylation of lipomodulin and release of arachidonic acid from peptide-stimulated neutrophils required Ca2+ entry into the cells. These results suggest that the phosphorylation-dephosphorylation of lipomodulin, phospholipase inhibitory protein, is an important mechanism for chemotactic receptor-mediated regulation of arachidonic acid release in rabbit neutrophils.
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PMID:The regulation of lipomodulin, a phospholipase inhibitory protein, in rabbit neutrophils by phosphorylation. 626 23

Fusion of human myeloma cell line GM 4672 and tonsillar lymphoid cells from a normal donor resulted in 13 primary hybridomas, which produced IgM anti-single-stranded DNA (ssDNA) antibodies, as determined in enzyme-linked immunosorbent assay. Nine of these primary hybridomas have been cloned and a total of 34 clones were obtained. Supernatants of these cloned hybridomas were tested for binding to ssDNA, native DNA, RNA, low molecular weight supernatant DNA, polydeoxyguanylate-polydeoxycitidylate, polydeoxyadenylate-thymidylate sodium salt, and cardiolipin. Supernatants from all clones but one showed polyspecificity when reacting with the antigens tested. That the clones were true hybridomas rather than transformed lymphoid cells was evidence by IgM anti-DNA antibody secretion, karyotype analysis, and HLA typing. These studies imply that immunoglobulin genes encoding for anti-DNA autoantibodies with a spectrum of nucleic acid specificities similar to systemic lupus erythematosus, exist among normal B lymphocytes.
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PMID:Anti-DNA autoantibody-producing hybridomas of normal human lymphoid cell origin. 647 Jan 43

The studies reported here were designed to determine whether sera from various patients could prevent neutrophils from responding to the lymphokine, neutrophil migration inhibition factor from T lymphocytes (NIF-T). Neutrophils from healthy donors were treated with sera from 84 subjects and assayed for responses to NIF-T. Serum from 7 of 37 patients (19%) with rheumatoid arthritis, systemic lupus erythematosus, and various forms of vasculitis showed blocking activity. In contrast, none of 47 subjects, including healthy individuals and patients with spondylarthropathies, cancer, and active infections had a serum factor that prevented neutrophils from responding to NIF-T (P less than 0.01). Serum blocking activity occurred transiently in association with infection by Staphylococcus aureus in one patient with rheumatoid arthritis. Moreover, autologous neutrophils from this same patient showed impaired responses to NIF-T. Blocking activity could be eluted from protein A-Sepharose in three of three patients studied. In three of seven patients, blocking activity was detected in serum cryoprecipitates, with a recovery of 46 to 78% of the blocking activity and overall enrichment (purification) of 137- to 281-fold. Analysis of cryoprecipitates by sodium dodecyl sulfate-polyacrylamide gel electrophoresis showed the predominance of immunoglobulins M and G. In one patient, the serum blocking activity was not cryoprecipitable, and cryoprecipitates from a patient with essential cryoglobulinemia failed to prevent neutrophils from responding to NIF-T. Blocking activity was relatively specific for NIF-T, as there was no effect on F-met-leu-phe-induced chemotaxis of neutrophils. Serum blocking activity in patients with connective tissue disease showed some correlation (r = 0.50; P less than 0.01) with immune complexes detected by polyethylene glycol precipitation but not Clq binding. These studies suggest that the response of neutrophils to NIF-T may be blocked by serum, possibly as a result of immune complexes or autoantibodies found primarily in patients with connective tissue disease.
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PMID:Impaired response of neutrophils to a lymphokine by sera from patients with connective tissue disease. 664 68


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