Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0409974 (lupus)
 22,386 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The C1q solid phase and Raji cell radioimmune assays were used to determine the frequency of detectable circulating immune complexes in patients with glomerulonephritis. In this study, 46% of 56 patients with glomerulonephritis had evidence of circulating immune complexes. More important, circulating immune complexes were associated with some, but not other, types of glomerulonephritis. Thus, immune complexes were detected in lupus glomerulonephritis (9/9 patients), rapidly progressive glomerulonephritis (5/6 patients), and acute nephritis (5/6 patients), but not in IgA-IgG glomerulonephritis (0/7 patients), or membranous glomerulonephritis (0/8 patients). The Raji cell radioimmune assay and the C1q solid phase radioimmune assay showed concordance of 79% in the detection of circulating immune complexes. Serial determinations, in general, showed either persistence of a negative or positive result of conversion of positive to negative.
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PMID:Application of the solid phase C1q and Raji cell radioimmune assays for the detection of circulating immune complexes in glomerulonephritis. 65 39

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

In order to analyze relation of immunological abnormalities to the development of lupus glomerulonephritis (LGN) at an early stage, various immunological parameters were examined in BXSB and MRL/lpr mice at 8 and 13 weeks of age. The following results were obtained. (a) Male BXSB mice showed slight LGN already at 8 weeks of age and the disease became obvious at 13 weeks of age. On the other hand, glomerular change of MRL/lpr mice became apparent at 13 weeks. (b) Immunofluorescent studies to semiquantify degree of the deposition of immune complexes (IC) at glomeruli revealed that there were no difference in fluorescence intensities among BXSB mice at 8 and 13 weeks and 13-week-old MRL/lpr mice. (c) MRL/lpr mice had much higher level of serum IC than male BXSB mice at 13 weeks as assessed by fluid- and solid-phase C1q-binding assays. Both strains showed almost the same level of Raji cell-binding IC which might be related to glomerular depositing ones. (d) Spleen of 13-week-old MRL/lpr mice contained extraordinary number of IgG-producing cells in spleen as compared with 8-week-old mice or male BXSB mice at 8 or 13 weeks. There were no differences in IgM-producing cell numbers among the strains and ages of mice. These results indicate that MRL/lpr and male BXSB mice have different immunological backgrounds for the development of LGN. It was noticeable that male BXSB mice showed some degree of LGN already at 8 weeks of age, without apparent polyclonal B cell activation and enhanced serum level of IC, as compared with MRL/lpr mice of the same age.
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PMID:Studies on the mechanisms of the development of lupus nephritis in BXSB mice. II. Comparative studies between male BXSB and MRL/lpr mice at the onset period. 325 31

A natural IgM monoclonal antibody, 1.67, was generated from apparently healthy unstimulated BALB/c mice. This antibody reacted with L5178Y murine T cell lymphoma, with human Raji cells, and with several normal cells. Further analysis of its ligand binding capacity disclosed strong binding to single-stranded DNA (ssDNA). However, this naturally-occurring monoclonal antibody binds to different epitopes on cell membranes and on DNA than another anti-DNA monoclonal antibody (18/103/1) from human origin. This conclusion was based on competition assays. Furthermore, NOA 1.67 lacks the 16/6 idiotype expressed on the 18/103/1 antibody. The 16/6 idiotype is shared by human and mouse lupus monoclonal autoantibodies that bind simultaneously to lymphoid cells and DNA. This is a first report on a natural autoantibody that binds to malignant and to normal cell membrane(s) as well as to ssDNA. It may have regulatory functions controlling malignancy and or autoimmunity.
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PMID:Naturally-occurring tumor-reactive autoantibodies: a monoclonal antibody from normal mice reacts with tumor cells and with DNA. 325 44

To determine the clinical significance of the Raji cell radioimmunoassay as a laboratory marker of activity, four patients with systemic lupus erythematosus (SLE) were followed for a period of 30 to 90 months. These sequential analyses did not show a correlation between circulating immune complexes, determined by Raji cell radioimmunoassay, and signs and symptoms in these lupus patients over a period of several years. We believe that the Raji cell test offers no advantage over other well known immunologic parameters used in SLE (antibodies to native DNA, complement factors C3 and C4 or CH50). In the management of SLE patients, laboratory data should not serve as a key by which to adjust treatment with prednisone or immunosuppressive drugs; clinical data are of outstanding importance in this respect.
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PMID:[Is the Raji cell test suitable as a marker of systemic lupus erythematosus activity? A case report]. 350 Nov 64

Seven of 60 human monoclonal anti-DNA autoantibodies derived from 3 patients with SLE were shown to bind to Raji cells by radioimmunoassay. The binding of the lupus autoantibodies to the Raji cells in solution was not affected by prior incubation of the cells with DNase. Preincubation of the monoclonal autoantibodies with polynucleotides and cardiolipin, resulted in significant inhibition which correlated with the direct binding characteristics of these antibodies. Previous results with mouse IgG monoclonal anti-DNA antibodies supported by our results with human IgM anti-DNA autoantibodies suggest caution in interpreting analyses of immune complexes of sera containing anti-DNA antibodies entailing Raji cells.
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PMID:Human lupus monoclonal autoantibodies bind to Raji cells. 408 63

Raji and Daudi are human B lymphoblastoid cell lines that readily form lupus inclusions (LIs; TRS) when grown in medium supplemented with leukocyte-, or fibroblast-derived interferon (IFN-alpha, -beta, respectively). WISH, MDBK, and GM2504 are three cell lines commonly used to measure antiviral activities. None of them form LIs in their antiviral response to alpha or immune (gamma)IFN. This distinguishes between the abilities of a cell to develop an antiviral state and to form LIs in response to IFN. Human (Hu) lymphoblastoid IFN and the two pure and homogeneous recombinant human IFN-alpha proteins IFLrA and IFLrD induce LIs in Raji cells and Daudi cells. In Daudi, a simultaneous inhibition of cell growth occurs. When compared by antiviral activities, IFLrA inhibits the growth of Daudi cells more, while IFLrD induces the greater frequency of LIs. According to molecular concentration, IFLrA and IFLrD at 133 X 10(-13) M induce LIs in Daudi cells to their maximum frequency. Growth inhibition for these same cell samples is also at maximum for IFLrA, but only 25% of maximum for IFLrD. Our results with Raji and Daudi cells provide evidence against a cause-and-effect relationship between these two biologic responses to IFN by Daudi cells. They also provide evidence for distinct, but interacting, intracellular pathways. This phenomenon is a new explanation for some of the biologic diversity shown for the HuIFNs-alpha.
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PMID:Purified recombinant human leukocyte interferons IFLrA and IFLrD induce human lupus inclusions in Raji and Daudi cells. 609 90

Raji cells, a human B lymphoblastoid cell line of Burkitt lymphoma origin, formed lupus inclusions when grown in a medium conditioned by the growth of Raji cells whose DNA thymidine residues had been unifilarly (single-strandedly) substituted with bromodeoxyuridine. Ultracentrifugation of this medium in excess of that required to remove Epstein-Barr virus and all other known mammalian viruses did not prevent the formation of the inclusions, and treatment of the conditioned medium with pronase destroyed the activity. These results demonstrate the presence of a protein that is secreted from bromodeoxyuridine-substituted Raji cells and is capable of inducing nonbromodeoxyuridine-substituted cells to form lupus inclusions. Interferon (100 units per milliliter) was found in the conditioned medium. Inclusions also formed in Raji cells grown in fresh medium supplemented with human leukocyte or fibroblast interferon (100 units per milliliter).
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PMID:Human lupus inclusions and interferon. 616 84

The La antigen recognized by certain lupus erythematosus autoantibodies was found to be predominantly associated with 7 S RNA in baby hamster kidney cells and human Raji cells, but not in HeLa cells where mainly the 7-2 RNA was associated with the La protein. In mouse myeloma cells (MPC-11) and mouse lymphoma cells (WEHI) that secrete immunoglobulins, equal amounts of 7 S and 7-2 RNAs were present in anti-La immunoprecipitates. The highly conserved 7 S RNA is a component of the signal recognition particle involved in protein secretion (Walter, P., and Blobel, G. (1982) Nature (Lond.) 299, 691-698), and its association with the La antigen appeared to be cell-type specific. Thus, it is possible that the La-7 S RNA association correlates with the abundance of 7 S RNA or with the secretory activity of the cell type.
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PMID:Association between the 7 S RNA and the lupus La protein varies among cell types. 619 54

C1q-precipitins (C1q-p) are comprised of 7S IgG with C1q-binding activity found in sera of patients with hypocomplementemic vasculitis urticaria syndrome ( HVUS ) and systemic lupus erythematosis (SLE). We have utilized C1q-coated polystyrene beads to selectively isolate C1q-p and to establish a sensitive and quantitative assay of C1q-p and immune complex activity. Purified C1q-p was comprised of polyclonal IgG which retained 7S sedimentation and solid phase C1q-binding activity at physiological ionic strength both in the presence and absence of normal human sera. No precipitation interaction was observed between C1q-p and fluid-phase C1q or C1 under the conditions tested. Purified C1q-p had no activity in the Raji cell immune complex activity. C1q-p activity also was observed in and purified from SLE serum; this activity was distinguishable from 7S immune complex activity detected by Raji cells which was also present in SLE serum. These studies indicate that C1q-p is a 7S IgG molecule found in HVUS as well as some SLE sera and has activity in C1q-binding but not in Raji cell-binding immune complex assays. These data also suggest that C1q-p is a monomeric, polyclonal IgG with preferential affinity for bound C1q. In addition to its potential role in immune complex disease, C1q-p may also provide an important tool for studying the interaction of immunoglobulin and C1q, and should contribute important information to understanding the pathobiology of immune complex disease.
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PMID:Assay, purification and further characterization of 7S C1q-precipitins (C1q-p) in hypocomplementemic vasculitis urticaria syndrome and systemic lupus erythematosus. 637 56


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