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)

An assay for circulating immune complexes is described which uses radiolabelled bovine conglutinin as ligand and polyethylene glycol precipitation as the technique for separating bound ligands. The technique is simple to perform and gives good sensitivity detecting artificial immune complexes. Its use in detecting complexes in systemic lupus erythematosus and Burkitt's lymphoma is described and it is compared with the Clq binding assay also performed with polyethylene glycol. It is suggested that the simultaneous performance of polyethylene glycol assays using radiolabelled Clq and radiolabelled conglutinin may be an advantageous method for screening sera for the presence of immune complexes.
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PMID:Conglutinin binding polyethylene glycol precipitation assay for immune complexes. 11 38

A characteristic alkaline phosphatase (orthophosphoric monoester hydrolase, alkaline pH optimum, EC 3.1.3.1) was detected in the sera of most patients with infectious mononucleosis, acute and chronic lymphatic leukaemia, non-Hodgkin's lymphoma, Burkitt's lymphoma and nasopharyngeal carcinoma. The enzyme was also present in the sera of nine out of 26 patients with cancer of the cervix. N-APase in these cases counted 30-100% of the total alkaline phosphatase activity. N-APase was absent from the sera of healthy individuals and of patients with acute and chronic granulocytic leukaemia, breast cancer, colon cancer, rheumatoid arthritis, ulcerative colitis, systemic lupus erythematosis, hepatitis and obstructive jaundice. Only three of 22 patients with Hodgkin's disease showed n-apase activity in the serum. In infectious mononucleosis the presence of N-APase activity was well correlated with the clinical course. In 13 cases studied, the clinical improvement was associated with the decrease or disappearance of N-APase activity. N-APase activity could not be detected in white cells of acute myeloid leukaemic patients, nor in the cells of myeloid blastic crisis of chronic granulocytic leukaemia. It was present in the cells of lymphoid blastic crisis of chronic granulocytic leukaemia.
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PMID:N-alkaline phosphatase: a potential disease marker for lymphoproliferative disorders. 43 2

The specific humoral response against polypeptide components of Epstein-Barr virus (EBV), the induced early diffuse antigen (EA-D), in patients with connective tissue diseases, including systemic lupus erythematosus (SLE) and mixed connective tissue disease (MCTD), was investigated by using the immunoblotting technique. The EA(D)-positive sera from patients with infectious mononucleosis (IM), nasopharyngeal carcinoma (NPC), immunocompromised patients (renal transplant recipients and patients with AIDS) as well as the EA(D)-negative sera from patients with Burkitt's lymphoma and from clinically healthy subjects served as controls. Seven major antigenic polypeptides with molecular weights of 33 kDa, 35 kDa, 52 kDa, 54 kDa, 56 kDa, 58 kDa, and 134 kDa were detected reproducibly by the EA(D)-positive reference sera and, in particular, by each of the NPC sera tested. The EA(D)-positive sera from the other groups showed various combinations of detection patterns and few samples reacted with all the major EA(D) polypeptides. Seventy-three percent of sera from SLE and 47% of sera from MCTD were found to react with EA(D). Sixty-one percent of sera from SLE vs. 5% from MCTD detected all the EA(D) polypeptides. These results could either reflect perturbations of the immune response linked to the autoimmune disease or suggest a possible pathogenic role of EBV.
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PMID:Antibody responses against polypeptide components of Epstein-Barr virus-induced early diffuse antigen in patients with connective tissue diseases. 217 36

Patients with systemic lupus erythematosus (SLE) appear to be at increased risk for development of neoplastic disease. We describe the case of a male teenager with SLE and Burkitt's lymphoma. His presentation was similar to that of an exacerbation of his underlying SLE. We believe this to be the first case of Burkitt's lymphoma in a patient with SLE. The association of SLE and malignancy, with emphasis on lymphoproliferative states, is discussed.
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PMID:Burkitt's lymphoma in a patient with systemic lupus erythematosus. 233 62

In order to investigate the genetic basis for natural anti-DNA immune responses, we isolated and sequenced the variable gene elements (VH and VL) encoding an anti-DNA antibody expressed by a human hybridoma of normal origin (Kim4.6) and compared these sequences with those reported for four other human anti-DNA antibodies. The Kim4.6 antibody leader and VH segments were identical in nucleotide sequence with the VH1.9III germ-line VH3 gene, and the Kim4.6VL segment showed 98% nucleotide sequence identity with a V lambda I subgroup gene expressed in a Burkitt's lymphoma. Comparative analysis of Kim4.6 and other human hybridoma anti-DNA antibodies indicated that anti-DNA immune responses are diverse in terms of VH and VL gene utilization but may exhibit a bias toward rearrangement of VH genes that are over-represented in the fetal pre-B cell repertoire. Moreover, Kim4.6 and three of four other sequenced human anti-DNA antibodies appear to use a germ-line diversity gene, DXP'1, which may represent a counterpart of the DFL16.1 segment utilized in murine responses to the hapten nitrophenyl. Taken together, our findings indicate that anti-DNA immune responses can be encoded by nonmutated VH genes and that the elements and molecular mechanisms which engender this response are essentially the same among natural and lupus-associated anti-DNA antibodies. Our data also suggest that natural autoimmune responses originate early in B cell ontogeny as is consistent with the hypothesis that autoreactivity plays a major role in shaping the normal immune repertoire.
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PMID:Analysis of variable region genes encoding a human anti-DNA antibody of normal origin. Implications for the molecular basis of human autoimmune responses. 278 10

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

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

Epstein-Barr virus (EBV) infection is associated with production of autoantibodies. The N-terminal 35-58 sequence of EBNA I, one of the nuclear antigens encoded by EBV, is highly homologous to the C-terminal 95-119 region of the ribonucleoprotein SmD. Autoantibodies specific for SmD are present only in systemic lupus (SLE) sera and are therefore considered a serological marker of SLE. We measured antibodies to the EBNA I 35-58 sequence in EBV-related diseases and in autoimmune disorders. Antibodies to the EBNA I 35-58 peptide were present in 30% of normal sera, 12% Burkitt lymphoma, 22% infectious mononucleosis, 25% rheumatoid arthritis, 38% SLE and 33% Sjogren's syndrome. Antibodies to the SmD 95-119 peptide were detectable in 32% of SLE sera, 17% infectious mononucleosis and 12% Burkitt lymphoma. The specificity of anti-EBNA I 35-58 antibodies affinity-purified from nine sera was analysed by means of an inhibition assay. Only anti-EBNA I 35-58 antibodies affinity-purified from SLE sera have a similar affinity for the viral peptide and the SmD C-terminal one; they also bind the recombinant SmD in western blot. The results indicate that antibodies to EBNA I 35-58 are produced in normals, in EBV-related diseases and in autoimmune disorder, but only SLE sera contain anti-viral antibodies cross-reactive with an autoantigen.
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PMID:Immune response to different sequences of the EBNA I molecule in Epstein-Barr virus-related disorders and in autoimmune diseases. 751 83

Mononuclear cells from the peripheral blood of patients with systemic lupus erythematosus (SLE) were transformed with the Epstein-Barr virus (EBV) and the resultant polyclonal B-lymphoblastoid cell lines were tested for antibody activity to membrane antigens of certain T-cell lines. B lymphoblastoid cell lines secreting specific antibodies were fused with (mouse x human) heteromyeloma SHM-D33 cells. Among the large number of hybridomas generated, one which produced a human monoclonal antibody (MAb) TONO-1 (IgM, lambda) was selected. MAb TONO-1 proved to be reactive with 4 human T-cell lines, HPB-MLT, L-MAT, MOLT-3 and MOLT-4F, but not with B-leukemia, Burkitt's lymphoma, myelomonocytic leukemia, erythroleukemia or non-hematopoietic malignant cell lines. MAb TONO-1 reacted positively with fresh leukemia cells from 2 of 7 patients with acute T-lymphocytic leukemia, but no reaction was observed in non-T-cell leukemia cases. Normal lymphocytes, monocytes, granulocytes, red blood cells and platelets in the peripheral blood did not demonstrate remarkable binding. Neither thymocytes nor bone-marrow cells from healthy volunteers were reactive. The antigens defined by MAb TONO-1 were polypeptides of 57 kDa and 68 kDa. Immunohistological studies revealed no staining of thymocytes in the thymus of a 6-month-old child, but showed epithelial reticular cells and Hassall's corpuscles to stain positively. These results suggest that MAb TONO-1 is directed to T-leukemic cells and some components of thymus tissue.
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PMID:A novel human monoclonal antibody, TONO-1, reactive with T-lymphocytic leukemia cells. 760 65

11111onglutinin-binding assay (KgBa) has gained widespread use for the detection of circulating immune complexes. A recent paper questioned the interpretation of the results obtained by this method and the validity of the assay (Holmskov et al. (1992) J. Immunol. Methods 148, 225). We now present hitherto unnoted differences between controls and patients with either rheumatoid arthritis or systemic lupus erythematosus. For this we use simple, but unconventional, graphic representations of the data, based on difference plots and ratio plots. Differences between patients with Burkitt's lymphoma and systemic lupus erythematosus from another previously published study (Macanovic, M. and Lachmann, P.J. (1979) Clin. Exp. Immunol. 38, 274) are also represented using ratio plots. Our observations indicate that analysis by regression analysis may often be misleading.
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PMID:Difference and ratio plots: simple tools for improved presentation and interpretation of scientific data. Unexpected possibilities for the use of the conglutinin binding assay in inflammatory rheumatic diseases. 783 83


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