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 sensitive crossed radioimmunoelectrophoretic method (CRIE), originally developed to study lymphocyte-associated beta 2-microglobulin (beta 2m), was applied in the study of serum beta 2m in patients with systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA). In six of seven patients with SLE and nineteen of twenty-seven patients with RA a considerable electrophoretic heterogeneity of serum beta 2m was found. In addition to the normally seen symmetric beta 2m precipitate, a beta 2m precipitate exhibiting complete immunochemical identity was found in the alpha-electrophoretic region. Binding of isolated 125I-labelled beta 2m to the abnormal precipitate was demonstrated in crossed immunoelectrophoresis. After gel filtration of sera exhibiting the above-mentioned beta 2m binding, all beta 2m was eluted in low molecular weight fractions corresponding to free beta 2m. By application of appropriate antisera and a glycoprotein-binding lectin in intermediate gels in CRIE, it was shown that the possible beta 2m-binding ligand is not an antibody, not a major constituent of normal human serum, and not unmodified HLA alloantigen. The abnormality was not restricted to patients with high disease activity but was found more frequently and was more pronounced (mean score 1.6 arbitrary units against 0.57 arbitrary units, P less than 0.01) in such patients. Thus our data exclude the possibility that autoantibodies to beta 2m were present in serum from patients with SLE and RA.
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PMID:Demonstration of electrophoretic heterogeneity of serum beta 2-microglobulin in systemic lupus erythematosus and rheumatoid arthritis: evidence against autoantibodies to beta 2-microglobulin. 8 1

A factor secreted by thymocytes of immunized rabbits totally suppressed both the initiation of, and ongoing synthesis and secretion of, lectin (PWM)-induced synthesis of IgM and IgG immunoglobulins by the circulating B lymphocytes of normal humans, and of twenty consecutive patients with rheumatoid arthritis and twelve consecutive patients with systemic lupus erythematosus. The suppressor factor, referred to as human Ig synthesis/secretion suppressor factor or HISSF, is not HLA restricted in its activity and is not cytotoxic to the circulating human mononuclear cells (B cells, T cells, Null cells and monocytes). It was demonstrated that T cells precultured with HISSF were transformed into suppressor cells which, when added to fresh cultures of autologous B cells, suppressed the synthesis and secretion of IgM and IgG. On the basis of its suppressive and non-cytotoxic properties in vitro, HISSF may be an effective immunosuppressant in the treatment of patients with autoimmune diseases.
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PMID:A non-cytotoxic suppressor of immunoglobulin synthesis and secretion by B cells of normal humans and patients with rheumatoid arthritis and systemic lupus erythematosus. 168 3

Vitamin A treatment (100,000 U daily) of systemic lupus erythematosus, non-Hodgkin's lymphoma and chronic lymphocytic leukemia patients, children suffering from recurrent respiratory tract infections and healthy controls resulted in an enhancement of antibody-dependent cell-mediated cytotoxicity, natural killer activity and blastogenic response to mitogens. In vitro, retinoids, depending on the concentration, stimulated mitogen- and interleukin-2-induced blastogenesis and lectin-dependent T cell cytotoxicity. Retinoids caused an early plasma membrane hyperpolarization of cells of various origin. This effect was similar to that seen by interferon alpha. Retinoids also slightly inhibited intracellular calcium accumulation.
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PMID:Immunological effects of retinoids. 171 57

A novel thermolabile beta-2 macroglycoprotein ('thermolabile substance' (TLS) or 'Hakata antigen' (HA], which was detected by the precipitating (auto) antibodies of patients with systemic lupus erythematosus, was isolated and characterized. The purification procedure entailed the following steps: isoelectric precipitation in the range between pH 5.2-6.1, hydroxyapatite absorption chromatography, 35% saturated ammonium sulfate precipitation, Sephadex G-200 gel filtration, Pevikon block electrophoresis, lentil lectin affinity chromatography and immobilized rabbit anti-human whole serum IgG column chromatography. Utilizing these procedures, 0.1 mg of HA was purified from 3 1 of pooled human serum. The molecular mass of HA was determined as 650 kDa by Sepharose 4B gel filtration. On SDS-PAGE analysis, HA showed a single band at 35 kDa under reduced conditions and numerous ladder bands between 35 kDa to more than 300 kDa under nonreduced conditions. On analytical ultracentrifugation, HA gave a molecular mass of 520 kDa with a single meniscus and a sedimentation constant of 12.0. The amino acid and carbohydrate analysis of reduced and S-pyridylethylated HA revealed that it contained five residues of hydroxyproline and an N-linked type sugar chain.
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PMID:Isolation and characterization of a thermolabile beta-2 macroglycoprotein ('thermolabile substance' or 'Hakata antigen') detected by precipitating (auto) antibody in sera of patients with systemic lupus erythematosus. 185 27

We have characterized a new antibody specificity in a panel of sera from dogs developing systemic lupus erythematosus (SLE) or clinically related autoimmune disorders. This antibody stains in a speckled fashion the nucleus of cells of different mammalian origins. The target antigen is a basic (pI 9.2) nuclear polypeptide with an apparent molecular weight of 43 kDa (p43) which is detected in various mammalian cell nuclei. p43, as studied in HeLa cells, appears to be cell cycle-independent. It is released from nuclei by salts (0.5 M NaCl or 0.25 M ammonium sulfate). Upon subfractionation of nuclear components, p43 is found in the fraction containing HnRNPs and is recovered in immunoprecipitates obtained with 4F4 monoclonal antibody to HnRNP C proteins. Immunoelectron microscopy revealed that p43 is concentrated over the dense chromatin periphery and interchromatin granule clusters. Another important feature of p43 is its ability to specifically bind wheat germ agglutinin lectin but not concanavalin A nor Ulex europaeus I, supporting the notion that p43 is a glycoprotein bearing an N-acetyl-glucosamine moiety. Consistent with this result, a radio-active p43 band is specifically immunoprecipitated by canine anti-p43 autoantibodies from HeLa cells metabolically labeled with [14C]glucosamine. Finally, anti-p43 antibodies do not immunoprecipitate SnRNA, indicating that p43 has no apparent association with SnRNPs.
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PMID:A novel 43-kDa glycoprotein is detected in the nucleus of mammalian cells by autoantibodies from dogs with autoimmune disorders. 199 2

We report a new antibody specificity in 15 sera recovered from a group of dogs developing systemic lupus erythematosus (SLE) or clinically related disorders. This antibody stains in a speckled fashion the nucleus of human Hep-2 cells. Immunodiffusion tests with saline extracts of rabbit thymus showed that all 15 sera generate a common precipitation line which crosses the lines from reference sera to Sm, SS-A/ro, SS-B/La, and RNP antigens. The target nuclear antigen is a 40 kD polypeptide (p40). An important property of p40 resides in its ability to bind specifically Wheat Germ Agglutinin lectin but not Concanavalin A, supporting the notion that the antigen is a glycoprotein bearing a N-acetylglucosamine moiety.
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PMID:[Serum antibodies in dogs with autoimmune disorders recognize 40 kd glycoprotein in the nucleus of mammalian cells]. 211 64

Quantitative changes of concanavalin A (Con A)-reactive proteins in serum samples obtained from rats with induced inflammation and from patients with inflammatory and autoimmune diseases were examined by use of lectin blots. Treatment of rats with a single dose of fermented yeast to induce inflammation caused an extensive increase in Con A-reactivity. These changes were time dependent and were similar in both sexes of the animals. When we examined serum samples obtained from patients with various inflammatory disorders for their Con A-reactive proteins as compared with normal donors, we noted that the Con A-reactivity increased in patients with rheumatoid arthritis and systemic lupus erythematosus. Among all the glycoproteins examined by lectin blots with use of Con A, a set of five proteins was selected for detailed analysis by densitometric scanning. These included alpha 2-macroglobulin, P-150, P-95, P-40, and P-35, of Mr 180,000, 150,000, 95,000, 40,000, and 35,000, respectively, by sodium dodecyl sulfate-polyacrylamide gel electrophoresis under reducing conditions. Densitometric scanning analysis of the lectin blots revealed that the Con A-reactivity of these proteins increased during inflammation. Because alpha 2-macroglobulin is not an acute-phase protein in humans, an increase in Con A staining of this protein suggested that altered glycation is associated with autoimmune diseases. Thus, study of changes in Con A-reactive proteins in human sera may facilitate our understanding of the etiology and pathophysiology of autoimmune diseases.
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PMID:Changes in concanavalin A-reactive proteins in inflammatory disorders. 247 95

We characterized the nuclear proteins with specific binding ability against c-myc gene by gel-shift assay in cell extracts of peripheral blood mononuclear cells (PBMC) from SLE patients and SLE-prone mice with use of distinct c-myc fragments. With the fragment named Fmyc in our experiments, two kinds of complexes which we call C1 and C2 respectively were found in PBMC from SLE patients and SLE-prone mice. The C1 was shown to be inducible in PBMC from healthy persons without nascent protein synthesis after lectin binding to the cell and found to be elevated in the SLE patients and in all of the established cell lines we examined. The C2 seemed to be peculiar to SLE subjects. The binding site of the C1 factor (C1F) and C2 factor (C2F) which forms C1 and C2 respectively with Fmyc appeared to be common and were found to reside at 51 kbp sequence (from XhoI to Sau3A) of exon I of c-myc gene. Interestingly, XhoI site of the binding site was highly demethylated in PBMC of SLE patients as compared with healthy persons. The roles of these binding factors for the pathogenesis of SLE are discussed.
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PMID:C-myc gene binding factors in peripheral blood mononuclear cells from patients with systemic lupus erythematosus (SLE). 277 56

Isoniazid (INH) and hydralazine (HYD) are transglutaminase (TGase, E.C.2.3.2.13.) substrates containing catalytically recruitable hydrazyl groups. Since they can be expected to inhibit TGase-mediated cell functions by competing with physiological substrates, their effect upon allogeneically and lectin-induced proliferation of mononucleocytes and upon zymosan-induced chemiluminescence of phagocytes was studied. Both compounds inhibited chemiluminescence in a dose-dependent manner. ID50 of HYD was consistently below 20 microM, while that of INH was above 120 microM. Proliferation of immunocompetent cells was suppressed by HYD with an ID50 of 60 microM, INH was inhibitory only above 5000 microM. Analogs of both compounds not containing hydrazyl groups proved to be inactive. Control experiments indicated that inhibition is not due to toxicity or lipophilicity of the compounds, structural analogs lacking a hydrazyl moiety were inactive. It is suggested that, in vivo, HYD interferes with signal-induced TGase-dependent leucocyte functions essential for immunologic stability, and that the resultant dysregulation with disruption of self tolerance contributes to the HYD promoted lupus-like syndrome.
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PMID:Effects of hydrazyl group containing drugs on leucocyte functions: an immunoregulatory model for the hydralazine-induced lupus-like syndrome. 286 61

Autoimmune New Zealand (NZ) mice exhibit a broad spectrum of T and B cell disorders. These include abnormally high levels of terminal deoxynucleotidyl transferase-positive immature T cells in bone marrow and thymus. We have shown previously that prostaglandin E1 (PGE1) treatment of the NZB/NZW F1 hybrid, a murine model of systemic lupus erythematosus (SLE), reduces to normal the percentage of immature terminal deoxynucleotidyl transferase-positive cells in bone marrow and thymus, and prevents the immune complex-induced nephritis which kills these animals. We report here that short-term (1-5 days) treatment of NZB/W mice with PGE1 increases thymocyte responsiveness to mitogens and alloantigens. The majority (greater than 90%) of cortical thymocytes agglutinated by peanut lectin (PNA+) are depleted by PGE1 treatment. However, a small population of highly functional cells persists in the PNA+ fraction after PGE1 treatment. PGE1 appears to have little or no effect on the PNA-negative (medullary) fraction of thymocytes. Our data suggest that PGE1 may exert its therapeutic effect in NZ mice by increasing the functional maturity of immature T cells.
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PMID:Effect of PGE1 treatment on in vitro thymocyte function of normal and autoimmune mice. 297 49


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