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)

Twenty-one sera from 11 patients with systemic lupus erythematosus were titrated with 125I-ss-calf thymus DNA to determine their maximum capacity to bind DNA. Only five sera were capable of binding greater than 90% of the input DNA. The remaining sixteen sera showed maximum DNA binding levels between 35% and 85%. The inability of these sera to bind all of the input DNA is shown to be dependent on variations in the molecular weight of the DNA antigen. The possibility that these differences in DNA binding reflect differences in antigenic specificity is discussed.
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PMID:Limited anti-DNA antibody specificity in systemic lupus erythematosus. 30 3

Immune complexe-like materials have been detected by a precipitation test with polyethylene glycol (PEG test) in the sera of 14 (93.3 p. 100) of 15 patients with active SLE, in 11 (44.0 p. 100) of 25 patients with inactive SLE, in 5 (83.3 p. 100) of 6 patients with widespread DLE and 3 (42.9 p. 100) of 7 patients with localized DLE. A good correlation was demonstrated between the value of PEG test and the complement consumption activity measured by an anticomplementary method in the cases of SLE, but it was not clear in the cases of DLE. The anticomplementary activity has been observed in the macromolecular fractions obtained by gel filtration on Sephadex G-200 of serum samples from one patient with active SLE and one patient with widespread DLE. As the value of PEG test had shown a tendency to increase with the antinuclear antibody titer if the titer was higher than 1 : 128, it is probable that the antinuclear factors were the important elements of the composition of circulating immune complexes in the cases of SLE. Contrarily, in several DLE patients, PEG test was positive despite lacking antinuclear antibody. In most cases, no significant decrease of PEG titers after DNase action was recorded, suggesting the participation of complexes containing antigens different from DNA.
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PMID:[Detection of circulating immune complexes in lupus erythematosus by precipitation test with polyethylene glycol and complement consumption test (author's transl)]. 30 93

Anti-DNA antibodies have been detected previously in patients with chronic discoid lupus erythematosus (DLE) despite the absence of overt systemic manifestations. 27 patients with DLE were followed up 3 years after the detection of anti-DNA antibodies in 7. None had developed other features of systemic lupus erythematosus. We conclude that the occasional finding of anti-DNA antibodies in patients with DLE does not predict those likely to develop systemic disease.
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PMID:Anti-DNA antibodies in discoid lupus erythematosus. Follow-up study. 30 2

The investigation of the fine specificities of antinuclear antibodies (ANAs) has been fruitful in terms of the nosology and immunopathogenesis of human autoimmune syndromes. Particular reactivities serve as "markers," in that patients with certain syndromes have a much higher incidence of such ANAs than do patients with other diseases. In this category is the almost exclusive against the nuclear acidic protein Sm. Reactivity to Sm can be detected by precipitation in agar, complement fixation, or passive hemagglutination (1,2). Autoimmune mouse strains have also provided a fertile field for the investigation of the basic phenomena of self-activity. In particular, the NZB strain and its hybrid NZB x NZW have been considered excellent models for human SLE and have therefore been studied in great detail (3,4). In addition, Murphy et al at The Jackson Laboratory, Bar Harbor, Maine, have developed several new inbred mouse strains that spontaneously develop SLE-like syndromes (5,6). These are the BXSB strain, which has a male dominant disease characterized by little antiative DNA antibody; the MRL/1, which develops massive, nonmalignant lymphadenopathy, associated with enormous increases in serum immunoglobulin levels and fulminant renal disease; and the MRL/n, which does not develop SLE-like disease until well into the 2nd yr of life, but like the MRL/1 develops high titers of ANA and fatal glomerulonephritis. The MRL/1 differs from MRL/n in only about 10 percent of its genome, including the gene responsible for the MRL/1's lymphoproliferation. In the current study, we have used the technique of double immunodiffusion (ID) in agarose with standard human reference sera (of known ANA specificity) to survey a large number of mice from the NZB x NZW, MRL/1, MRL/n, BXSB, and other strains. We report here the finding of the anti-Sm marker" antibody almost uniquely in MRL/1 and MRL/n animals. These two related strains may serve as experimental models to explore the mechanism stimulating the production of this unique autoantibody in SLE.
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PMID:Presence of anti-Sm reactivity in autoimmune mouse strains. 30 83

Administration of thymosin fraction V to NZB/NZW F1 mice, an animal model for human SLE, accelerated the appearance of proteinuria and anti-nDNA antibodies, increased deposition of immunoglobulins in kidneys, and significantly shortened survivals. Although the addition of thymosin to in vitro cultures of spleen and lymph node cells from thymosin-treated mice increased DNA synthesis in response to stimulation with Con A, in vivo treatment with thymosin did not affect the Con A response. There was no effect on in vitro responses to PHA or LPS, or on IgM antibody formation to SRBC (T cell dependent) or SSS III (T cell independent) immunizations. Antibodies to thymosin or contamination of our thymosin preparations with nucleic acids could not be demonstrated. The acceleration of autoimmune disease produced by thymosin treatment could not be explained by alteration of the T and B cell functions studied.
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PMID:Effect of altered lymphocyte function on immunologic disorders in NZB/NZW mice. III. Acceleration of disease by thymosin. 30 81

Anti-DNA antibody determination in serum is increasingly used because it supports the diagnosis of systemic lupus erythematosus (SLE) with high selectivity. The present work evaluates several of the technical variables of the Farr radioimmunoassay for anti-DNA antibody determination and describes a recommendable procedure, emphasizes the most important sources of error and gives the range of normal blood donors and a group of hospital patients without SLE.
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PMID:Anti-DNA antibody in serum measured by radioimmunoassay (Farr technique). Description of method and recommended procedure. 30 11

Serologic studies were performed on 25 patients with systemic lupus erythematosus (SLE) during 29 acute episodes of central nervous system (CNS) disease. Increased anti-DNA antibody and decreased total serum hemolytic complement activity were observed only in those patients with associated extra-CNS disease manifestations. Patients with isolated CNS disease were otherwise in apparent clinical and serological remission regarding these two indices. No special association of cold-reactive IgM antilymphocyte antibodies was demonstrable in patients with ongoing CNS injury. Of special interest was an increased incidence of anti-Sm antibodies in the patients with CNS dysfunction relative to that in a large group of patients without neuropsychiatric disease. The incidence of anti-RNP was not increased. The data do not support direct involvement in SLE brain injury of either DNA/anti-DNA complexes or of lymphocytotoxic antibodies cross-reactive with brain cells, but do suggest an association of anti-Sm with CNS disease in this disorder.
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PMID:Serologic studies in patients with systemic lupus erythematosus and central nervous system dysfunction. 30 51

Serial measurements were made over a period of three years of serum DNA-binding capacity and complement C3 and C4 levels in parallel with documentation of clinical features of disease activity in Glasgow patients with SLE. Raised DNA-binding levels were noted in 27 of the 32 patients over this time period. High levels (over 80%) were found in patients with both renal and non-renal disease. In some patients increases in DNA-binding capacity and decreases in C3 levels were associated with changes in disease activity. This pattern was commonest in patients with renal SLE. In others DNA-binding capacity was elevated without any relationship to SLE disease activity. A fall in serum C3 levels was usually significant while serum C4 levels frequently fell without any change in clinical features of disease activity. Very low serum C4 levels (below 15 mg/dl), however, were usually of clinical relevance. The uses of immunological measurements in the differential diagnosis of a major illness in a patient with SLE are discussed. The finding of such an illness in a patient with normal serum DNA-binding levels made it unlikely that the illness was due to an exacerbation of the SLE and more likely that an alternative cause such as supervening bacteraemia was responsible.
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PMID:The significance of serial measurement of serum anti-native DNA antibodies and complement C3 and C4 components in the management of patients with systemic lupus erythematosus. 30 17

The double-antibody solid-phase assay for DNA antibodies permits simultaneous and quantitative determination of antibodies to dsDNA and ssDNA. Using this method, 170 sera, mainly ANA-positive, were examined for the presence of anti-dsDNA and anti-ssDNA to assess the role of these antibodies in the ANA reaction. It was found that in the SLE group of patients, their ability to respond to dsDNA was correlated with the multiorgan symptomatology of disease. Anti-ssDNA titres are also highest in this group. However, anti-ssDNA titres predominate over anti-dsDNA in other collagen diseases. This predominance increases as we progress from the SLE group to undefined mild collagenosis, because the response to dsDNA decreases more than the response to ssDNA. This observation suggests that the clinical manifestation of the collagen diseases and multiorgan manifestation of SLE is linked with the pattern of response to DNA in the majority of cases. In conclusion, it appears that the determination of both ssDNA and dsDNA antibodies can be of value for the prognosis and management of patients with connective tissue disease.
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PMID:Evaluation of the simultaneous estimation of anti-dsDNA and anti-ssDNA antibodies for clinical purposes. 30 5

Anti-ENA antibodies have been found in 176 sera which nearly all contained antinuclear antibodies giving a speckled pattern of nuclear fluorescence. The charts of 134 of these 176 patients were available for a thorough clinical study. Among these 134 patients, 59 had a well defined Connective Tissue Disease including 40 SLE, 31 had a limited clinical syndrome made of Raynaud's phenomenon, inflammatory polyarthritis, swollen fingers and hyperglobulinemia and 34 had a complex clinical picture associating signs of more than one connective tissue disease. Some of the patients in this third group could be considered as-having the Mixed Connective Tissue Disease (MCTD) described by Sharp et al. Anti-RNP antibodies were more common in this series than the other anti-ENA antibodies. However, no narrow specificity could be assigned to any of these antibodies. This is true of the non anti-RNP antibodies, the anti-Sm in particular, which were found in 49 patients of whom 32 had SLE existing alone or in association with features of other connective tissue diseases and 17 had another connective tissue disease or the afore-mentioned limited clinical syndrome. In any case, the anti-ECT antibodies never reach the diagnostic value of the anti-DNA antibodies.
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PMID:[The clinical significance of soluble nuclear antigen specific antibodies (author's transl)]. 30 37


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