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)

The level and avidity of anti-DNA antibody in the serum of New Zealand Black/White (NZB/W F1) hybrid mice has been determined. The results show that there is an age and sex-related variation in the avidity of this antibody. In mice of both sexes, the avidity of circulating anti-DNA antibody increases up to 5 months of age; thereafter the avidity falls with increasing age. These variations are more marked in males, but female mice consistently have lower avidity anti-DNA antibody than males. Thus the time of onset, time course and severity of the murine lupus syndrome in NZB/W F1 mice are associated with the presence of increasing levels of low avidity anti-DNA antibody in the serum. These results are discussed in the context of the possible role of low avidity antibody in immune complex disease.
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PMID:The role of low affinity antibody in immune complex disease. The quantity of anti-DNA antibodies in NZB/W F1 hybrid mice. 12 30

A total of fifty-five biopsies from fifty-two intradermal DNA skin tests were studied. The biopsies were taken, 6, 8-10, 24 or 48 h after the injection of the DNA material. Necrosis of the vessel wall was taken to be the main characteristic of a specific reaction. In forty of the fifty-two tests the results of the histological evaluation closely matched the clinical results. In five of the fifteen cases with discrepancies, the histological evaluation ruled out clinically false positive test results. In three cases of SLE on corticosteroid treatment, the histological examination gave a positive result despite a clinically negative result. In seven of the fifteen cases the discrepancies occurred in borderline cases with reactions of 5 to 6 mm diameter. The amount of inflammatory cells in positive as well as in negative reactions was also recorded. The number of polymorphonuclear cells in positive reactions increased with the age of the reaction. The number of lymphocytes was not found to increase in the positive reactions, thus differing from the delayed hypersensitivity type of reactions. Rather, the reaction was characterized by an Arthus type of hypersensitivity. On the basis of the present study it may be concluded that clinically positive tests at 6 or 8 h may merely be expressions of nonspecific vascular alterations. On the other hand, in late reactions, even in patients on systemic treatment, histological examination revealed clinically negative results to be positive. By using the histological picture of hypersensitivity angiitis as the main diagnostic criterion the specificity of the clinical reactions may be established.
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PMID:The deoxyribonucleic acid (DNA) skin test in systemic lupus erythematosus. 2. Histological findings. 12 5

A method for the detection of native anti-DNA antibodies in serum is described. The method is based on the reactivity of fluorescein isothiocyanate with DNA, forming a complex capable of combining with anti-DNA antibodies. The fluorescein content of the precipitated fluorescein-DNA anti-DNA complex is then measured in a fluorometer. The assay is accurate, highly reproducible, and inexpensive to perform. Comparative studies performed with the Farr assay show the fluorimetric method to be more sensitive in detecting anti-DNA antibodies in the serum of SLE patients.
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PMID:Fluorimetric method for the detection of anti-DNA antibodies in serum. 13 37

The avidity of antibodies to DNA in the sera of 8 patients with SLE was determined by saturation analysis and Scatchard plots. Five of the patients had severe lupus nephritis; the other 3 had relatively mild or no kidney disease. The Scatchard plots revealed components with high relative avidity in the patients with severe nephritis (K values 4.4-10.4 X 10(5) M-1 for nDNA), compared with the patients who had mild or no kidney disease (K values 0.3-1.8 X 10(5) M-1 for nDNA). Avidity measurements may be helpful in the evaluation and treatment of patients with SLE.
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PMID:Avidity of antibodies in SLE: relation to severity of renal involvement. 13 25

The formation of anti-DNA antibodies appears to be under a genetic control similar to that regulating the immune response to complex antigenic compounds. The ability to develop a high immune response to DNA seems to be predominantly dependent on the nature of the B-cell population whereas a major role of the T-cell suppressor population is not evident in this response. The immune response to DNA does not necessarily need the presence of thymus-derived lymphocytes, but in some cases T-cells may exert a helper effect. The development of anti-DNA antibody response may be triggered by various factors: viral, bacterial or parasitic agents, tissue destruction or some drugs. A mechanism that may play an important role is the "nonspecific" triggering of anti-DNA antibodies by substances that, like bacterial lipopolysaccharides, exert a potent stimulatory effect on B-cells and simultaneously induce a release of DNA in extracellular fluids. In lupus diseases as well as in mice injected with lipopolysaccharide, pathogenic effects of anti-DNA antibodies appear to be closely related to the formation of DNA-anti-DNA complexes. The demonstration that injections of lipopolysaccharide lead to the localization of DNA-anti-DNA complexes in kidney glomeruli stressed the possible importance of stimuli responsible for a release of DNA in circulating blood in the expression of the pathogenic effects of anti-DNA antibodies.
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PMID:Genesis and pathogenicity of anti-DNA antibodies. 13 82

Detection of antibody to double-stranded DNA by direct binding assays has proved useful in clinical management of patients with systemic lupus erythematosus (SLE). Recent confusion regarding specificity of these antibodies for SLE appears to be due, at least in part, to contamination of natural DNA preparations with nondouble-stranded DNA antigens. Measurement of binding of a synthetic, self-complementary DNA copolymer (dAT) rather than of natural DNA (KB) has been shown to obviate some of these difficulties, apparently because of freedom of dAT from nondouble-stranded DNA antigens. Among the advantages found in this way was a higher degree of specificity of antibodies to double-stranded DNA for clinically-judged active lupus nephritis than had been suspected. Since activity of nephritis is difficult to assess clinically, histologic data were sought to confirm these observations. Thirty-two kidney specimens were examined by light and/or electron microscopy. The degree of histologic activity and the amount and location of glomerular electron-dense deposits were semiquantitated blindly. The binding of both dAT and KB DNA was measured by the ammonium sulfate method. Correlation with the amount of electron-defense deposits was highly significant for dAT binding and somewhat less so for KB DNA binding as determined by both parametric and nonparametric statistical methods. Significant correlation with histologic activity was found for dAT but not KB DNA binding. These results are consistent with previous data and suggest that dAT binding may provide a useful, noninvasive means of clinically assessing both nephritis activity and the intensity of glomerular immune-complex deposition as reflected by the amount of electron-dense deposits. If it can be confirmed that the latter provides long-term prognostic information, then dAT binding (and perhaps its reponse to therapy) may also prove of value in this regard.
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PMID:Binding of synthetic double-stranded DNA by serum from patients with systemic lupus erythematosus: correlation with renal histology. 13 6

The clinical features of 78 patients with SLE seen in Cairo and Glasgow are reviewed. Raynaud's phenomenon was recorded more frequently here than in previous series. The value of serial measurements of anti-DNA antibodies, C3 and C4 in the management of SLE is discussed. Although antibodies to native DNA paralleled the disease course in only a minority of SLE patients anti-DNA antibodies were present during all major SLE exacerbations and could be diagnostically useful. Serious systemic infections complicating the management of SLE patients could occur and their diagnosis is discussed.
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PMID:The clinical manifestations of systemic lupus erythematosus: a Cairo-Glasgow co-operative study. 14 Apr 59

Plasma postheparin lipolytic activity (PHLA) was measured on 50 patients with systemic lupus erythematosus (SLE). Plasma PHLA was significantly decreased in SLE patients. This decrease was most striking in the acute phase of the disease. There was a close relationship between decreased PHLA and immunologic factors indicative of the acute phase of SLE. These immunologic factors included shaggy antinuclear antibody pattern, low serum complement titer, high DNA antibody titer, mixed cryoglobulin and lumpy glomerular pattern by immunofluorescent staining.
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PMID:Decreased plasma postheparin lipolytic activity in systemic lupus erythematosus. 14 3

A patient is described with systemic lupus erythematosus and large painless ascites and pleural effusions. Pleural and peritoneal fluid complement levels were depressed, and DNA binding was elevated in the presence of normal serum values. Immunoglobulin and complement deposits were demonstrated in vessels of the pleura, peritoneum, and skin, along with histologic evidence of vasculitis. The relation of the ascites and pleural effusions to the presence of widespread vasculitis and local immune complex formation is discussed. These complications responded poorly to corticosteroid therapy but slowly resolved following the addition of an immunosuppressive agent.
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PMID:Immune complex vasculitis as a cause of ascites and pleural effusions in systemic lupus erythematosus. 14 41

Co-culture of autologous T and mitomycin-C treated B cells results in increased DNA synthesis in the responding T cells. T cells thus activated in AMLC exerted suppressive effects on both the proliferative and cytotoxic responses of fresh unstimulated T cells to allogeneic cells in MLC. The suppressor cells generated are sensitive to treatment with mitomycin-C. AMLC-activated cells treated with mitomycin-C failed to suppress both cytotoxicity and proliferation in fresh primary MLC. It appears that the AMLC reaction reflects an immunologic homeostatic mechanism. Since this reaction is defective in patients with CLL and SLE and the homologous mouse syngeneic MLC is defective in NZB mice, the failure of this T-B interaction may be related to the pathogenesis of certain lymphoproliferative and autoimmune disorders.
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PMID:Activation of suppressor T cells in human autologous mixed lymphocyte culture. 15 35


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