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)

Antibodies to soluble ribonucleoprotein (sRNP) are by definition a prerequisite for the diagnosis mixed connective tissue disease (MCTD). They are also found in 30--40% of other rheumatic conditions with a high titred speckled IFL reaction. The same is true for the most characteristic clinical features of MCTD, viz. Raynaud's syndrome and polymyositis--polymyalgia. The serological and clinical symptoms mentioned are closely associated. An association between anti-Sm and the SLE symptoms butterfly erythema, nephropathia, other visceropathias and cerebrovascular disease is confirmed by the present study. Although anti-Sm has less diagnostic specificity for SLE than has anti-ds-DNA, it is useful as a diagnostic aid in SLE cases lacking the latter antibody. The results of the present study tend to support the hypothesis that anti-sRNP may be associated with a prophylactive effect against serious vasculitis and nephropathia. When anti-sRNP and anti-Sm occur together they seem to act competitively so that the symptom associated with the antibody having the highest titre tends to dominate the clinical picture. Both anti-sRNP and anti-Sm produce speckled nuclear patterns in the indirect immunofluorescence test. Sera with immunofluorescence titres below 1/25 were not found to react against either sRNP or Sm. On the other hand all sera tested that had a speckled IFL reaction greater than or equal to 1/800 also had anti-sRNP.
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PMID:Symptomatology and diagnosis in connective tissue disease. II. Evaluations and follow-up examinations in consequence of a speckled antinuclear immunofluorescence pattern. 36 40

We examined the effects of gamma-interferon (gamma-IFN) and the new immunosuppressant FK506 on resting B cell proliferation of New Zealand black/white F1 hybrid (B/W F1) mice, an animal model of human systemic lupus erythematosus (SLE). gamma-IFN and FK506 inhibited in a dose-dependent manner both B cell proliferation and autoantibody production of resting B cells respectively. There was a synergistic interaction between gamma-IFN and FK506 in their inhibition and they did not exhibit cell cytotoxicity. This in vitro synergism of gamma-IFN and FK506 may have clinical application in that low doses of gamma-IFN and FK506 combinations may be effective to correct polyclonal B cell activation of patients with SLE.
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PMID:Effects of gamma-interferon and FK506 on resting B cell proliferation of New Zealand black/white F1 mice. 128 97

To gain insight into the immunopathogenesis of drug-induced autoimmune disorders, lymphocyte and immunoglobulin distributions and cytokine levels were monitored in the peripheral blood and pleural fluid of a patient with procainamide-induced lupus and pleural effusion. Approximately 80% of the B cells in both compartments were CD5+ compared to 10% to 25% in normal adults. CD4/CD8 ratio and percentage CD4 were normal in peripheral blood. Serum levels of IgG (particularly IgG2), IL-6, and soluble IL-2R were slightly elevated, and those of IgA were significantly elevated compared to normal controls. Analysis of the pleural effusion revealed an increased CD4/CD8 ratio because of an increased percentage of CD4+CD29+ helper memory T cells, lack of expression of the resting B-cell marker CD21, immune complex deposition and complement consumption, increased relative levels of ANA, abnormally high levels of IL-6 and soluble IL-2R, and detectable levels of IL-1b, IFN-g and TNF-a. These observations provide evidence for the involvement of CD5+ B cells and differential helper T-cell activity in procainamide-induced lupus and for an association between local lymphocyte activation and organ pathology.
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PMID:Case report: distinctive immune abnormalities in a patient with procainamide-induced lupus and serositis. 137 40

Whether inflammatory bowel diseases (IBD) can be classified as autoimmune disorders is not established. Since circulating acid-labile interferon-alpha (IFN-alpha) is believed to reflect autoimmune reactions, we tested sera from two groups of IBD patients for the presence of circulating IFN. No detectable IFN was found in 51 serum samples of IBD patients. Furthermore, in no serum sample of IBD patients were neutralizing anti-IFN antibodies found. In contrast, acid-labile IFN-alpha was present in sera from 21/52 HIV-infected and from 6/14 systemic lupus erythematosus patients. These observations provide evidence that IBD differs from systemic autoimmune disorders, at least for the presence of circulating IFN.
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PMID:Absence of circulating interferon in patients with inflammatory bowel disease. Suggestion against an autoimmune etiology. 138 5

Expression of MHC-class II molecules (HLA-DR and -DQ), serum gamma-interferon (gamma-IFN) and soluble interleukin-2 receptor (sIL-2R) levels were studied in 35 Japanese patients with lupus nephritis (LN) to clarify intraglomerular cellular activation and cytokine involvement in human LN. In 11 normal kidney specimens, HLA-DR(Ia1) was noted in glomerular tufts, but HLA-DQ was either not or was faintly detected in glomeruli by the indirect immunofluorescence technique. HLA-DR and -DQ were observed mainly on the surface of glomerular endothelial cells in 100% and 50% of 28 lupus kidney specimens except for necrotic or sclerotic lesions. HLA-DQ was expressed in a high incidence of 67%, 86% in patients with proliferative LN (WHO Class III-IV) and active lesions, respectively. Serum gamma-IFN and sIL-2R levels were 1.2 +/- 0.2 U/ml and 190 +/- 24 U/ml (mean +/- SEM; N = 30) in normal controls, and elevated in patients with proliferative LN (4.1 +/- 1.0 U/ml, 383 +/- 81 U/ml, N = 25), especially with active lesions (6.2 +/- 1.5 U/ml, 500 +/- 110 U/ml, N = 14). Overall, glomerular lesions such as HLA-DQ expression, the activity index and leukocyte infiltration correlated positively with serum gamma-IFN levels (r = 0.55; P less than 0.01 for HLA-DQ, r = 0.68; P less than 0.001 for activity index, r = 0.38; P less than 0.05 for leukocyte infiltration), but not with serum sIL-2R levels, anti-DNA antibody titers and CH50 titers.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Up-regulated MHC-class II expression and gamma-IFN and soluble IL-2R in lupus nephritis. 140 53

On the basis of the research on the relationship between human cytomegalovirus (HCMV) infection and systemic lupus erythematosus (SLE) a study of the effects of HCMV infection on the immunological pathogenesis of SLE was undertaken. Presented in this paper is a brief account of the study. It was found that SLE patients with active HCMV infection had significant higher level of serum interferon-alpha (IFN-alpha) than those without active HCMV infection, but the IFN-alpha induction capacity of peripheral blood mononuclear cells (PBMC) from SLE patients with active HCMV infection was evidently poorer than that from patients without it. There was not any statistically significant difference between the two SLE groups in the IFN-gamma induction capacity of PBMC.
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PMID:Immunomodulation of human cytomegalovirus infection on interferon system in patients with systemic lupus erythematosus. 166 8

Interferon-alpha (IFN-alpha) is currently used in the treatment of various malignant tumours. Development of different autoimmune disorders has been reported in some patients during IFN-alpha therapy. Systemic lupus erythematosus (SLE) after treatment with IFN-alpha has not been described, although a majority of SLE patients have demonstrable serum levels of IFN-alpha, which correlate with disease activity and have been suggested to be of pathogenetic significance. In this paper we describe a patient with a malignant carcinoid tumour who developed a SLE-like syndrome during treatment with leucocyte IFN-alpha. The patient developed myalgia and low grade arthritis in multiple joints together with a high titre of antinuclear antibodies (ANA) and anti-dsDNA antibodies. After the treatment was stopped, the symptoms subsided although a moderate ANA titre persisted. However, the tumour continued to regress despite cessation of IFN-alpha therapy. During a short course with recombinant IFN-alpha the syndrome relapsed, supporting the concept that the SLE syndrome was precipitated by IFN-alpha. A connection between IFN-alpha treatment, the induced autoimmune disorder and regression of the carcinoid tumour is suggested.
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PMID:Possible induction of systemic lupus erythematosus by interferon-alpha treatment in a patient with a malignant carcinoid tumour. 169 Feb 58

Several previous reports suggest an association between treatment of patients with interferon-alpha (IFN-alpha) and development of autoantibodies and autoimmune disease. We here summarize the experience from a group of 135 patients with midgut carcinoid tumors treated with natural leukocyte IFN-alpha or recombinant IFN-alpha (rIFN-alpha). An unusual high incidence of antimicrosomal antibodies (MsAb) or anti-thyroglobulin antibodies (TgAb) and thyroid disease manifested as hyperthyroidism, hypothyroidism or a biphasic Hashimoto-like disease was seen, with female predominance. The incidence of antinuclear antibodies (ANA) was also increased, but equally in both sexes. Antibodies to parietal cells were found in 5 cases and 4 patients with pernicious anemia were detected. Two patients developed vasculitis of leukocytoclastic type and one a syndrome resembling systemic lupus erythematosus. Some patients treated with rIFN-alpha develop anti-IFN antibodies. Such antibodies may also be autoantibodies reacting with autologous IFN-alpha. They can neutralize the biologic activity of administrated IFN preparation and cause therapeutic failure. The implications of the various autoimmune manifestations during IFN-alpha treatment are discussed.
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PMID:Autoimmune phenomena in patients with malignant carcinoid tumors during interferon-alpha treatment. 185 11

A 19-year-old man with Philadelphia-positive chronic myelogenous leukemia treated with interferon-alpha (IFN-alpha) therapy for 45 months had systemic lupus erythematosus disease features: malar rash, migratory arthralgias, elevated antinuclear antibodies, elevated antinative DNA, hypocomplementemia, lymphopenia, and proteinuria. After discontinuation of the IFN and initiation of corticosteroids, there was gradual recovery of symptoms, a decline in antinative DNA and antinuclear antibodies to normal levels, and a decrease in proteinuria. The potential association between IFN therapy and the development of systemic lupus erythematosus, and the role of IFN in other autoimmune diseases, is discussed.
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PMID:Development of systemic lupus erythematosus after interferon therapy for chronic myelogenous leukemia. 189 53

Recently, naturally occurring antibodies to IFN-alpha were discovered in a few systemic lupus erythematosus (SLE) and cancer patients; however, in most patients monitored for anti-IFN antibodies before treatment, no antibodies were found. In an attempt to explain the 'IFN-blocking effect' that we observed in all serum samples we investigated 200 sera from healthy blood donors. We isolated the globulin fraction, and used rabbit anti-human IgG and IgM columns, protein A columns and T-gel affinity chromatography to isolate human IgG and IgM. All sample fractions were tested in a biological IFN neutralization assay by means of a sensitive MTT-assay. We found that normal human serum contained autoantibodies to crude human leucocyte IFN, native human fibroblast IFN, recombinant human leucocyte IFN-alpha 2b and recombinant human IFN-gamma, and that these naturally occurring antibodies were biologically active immunoglobulins of IgG and IgM type. These anti-IFN antibodies were also present in purified human normal immunoglobulin pools. We conclude that all humans have naturally occurring anti-interferon antibodies in their serum, and it is a tempting theory that human cytokines and lymphokines are, at least partly, regulated by immunoglobulins.
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PMID:Autoantibodies to crude human leucocyte interferon (IFN), native human IFN, recombinant human IFN-alpha 2b and human IFN-gamma in healthy blood donors. 211 20


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