Measurement of anti-DNA antibodies: a reappraisal using five different methods.

Isenberg, David; Dudeney, C; Williams, Warren; Addison, I E; Charles, Séverine; Clarke, James S.; Todd-Pokropek, A

doi:10.1136/ard.46.6.448

Cited by 103 publications

(57 citation statements)

References 26 publications

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“…but the prevalence of renal disease was comparable. In this study, the Farr assay, using '2SI-labeled recombinant dsDNA, proved to be the most sensitive assay for anti-dsDNA antibody, which is in accordance with a recent report (29). Exacerbations, especially those with renal involvement, occurred more frequently in the group of patients who were positive for anti-dsDNA antibodies.…”

supporting

confidence: 91%

Measurement of increases in anti‐double‐stranded dna antibody levels as a predictor of disease exacerbation in systemic lupus erythematosus

Borg

Horst

Hummel

et al. 1990

Arthritis & Rheumatism

507

227

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To evaluate the predictive power of changes in levels of antibodies to double-stranded DNA (antidsDNA) as a predictor of disease exacerbations in systemic lupus erythematosus (SLE), we performed a prospective study on 72 unselected patients with SLE (mean duration of study 18.5 months, range 6-35 months). Patients were seen at least once every 3 months, and disease activity was scored according to a specific protocol. Plasma samples were obtained at least once every month and were assessed for anti-dsDNA antibody (by the Crifhidiu luciliue assay, an enzymelinked immunosorbent assay [ELISA], and the Farr assay) and for complement components C3 and C4. Twenty-seven of 33 disease exacerbations observed during the study period were accompanied by a positive test result for anti-dsDNA antibody (27 by the Farr assay, 19 by the C luciliae assay, and 23 by the ELISA). Twentyfour of these exacerbations were preceded by a significant increase in anti-dsDNA antibody levels (23 by the Farr assay, 12 by the C luciliae assay, and 17 by the ELISA). The first observance of a significant increase in anti-dsDNA antibody levels preceded the exacerbation by 8-10 weeks. Significant increases in anti-dsDNA antibody levels not followed by an exacerbation were observed in 5 cases by the Farr assay, in 7 cases by the C luciliue assay, and in 3 cases by the ELISA; however, in 3 cases, 2 cases, and 1 case, respectively, these increases were followed by an increase in disease activity that did not fulfill the criteria for an exacerbation. Serial measurement of anti-dsDNA antibody levels was more sensitive for predicting exacerbations than was measurement of C3 andor C4 levels (P < 0.03). Serial assessment of anti-dsDNA antibody levels, especially by the Farr assay, is a sensitive and reasonably specific method for predicting disease exacerbations in SLE.Systemic lupus erythematosus (SLE) is characterized by protean clinical manifestations and the occurrence of a variety of autoantibodies. Among these, anti-double-stranded DNA (anti-dsDNA) antibodies are highly specific for SLE and are detected at a high frequency (75-

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supporting

confidence: 91%

Measurement of increases in anti‐double‐stranded dna antibody levels as a predictor of disease exacerbation in systemic lupus erythematosus

Borg

Horst

Hummel

et al. 1990

Arthritis & Rheumatism

507

227

View full text Add to dashboard Cite

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“…Anti-ssDNA antibodies were detected by enzyme-linked immunosorbent assay (ELISA), as described previously [40], with minor modifications. Briefly, polyvinylchloride 96-well plates were precoated with 50 μl of poly-l-lysine (Sigma) by a 1-h incubation at 37°C.…”

Section: Analysis Of Serum Anti-dna Antibodies and Anti-rnp/sm Antibomentioning

confidence: 99%

Effects of adjuvants for human use in systemic lupus erythematosus (SLE)-prone (New Zealand black/New Zealand white) F1 mice

Favoino

Favia

Digiglio

et al. 2013

Clinical and Experimental Immunology

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SummaryThe safety of four different adjuvants was assessed in lupus-prone New Zealand black/New Zealand white ( Mean mouse weight at week 18 was lower in the ALU group than the IFA (Tukey's HSD post-test P = 0·04), CFA (P = 0·01) and SQU (P < 0·0001) groups, while the mean weight in the SQU group was higher than in the IFA (P = 0·009), CFA (P = 0·013) and UNT (P = 0·005) groups. The ALU group weight decreased by almost half between weeks 29 and 31, indicating some toxic effect of ALU in the late post-immunization period. Thus, SQU was the least toxic adjuvant as it did not (i) accelerate proteinuria onset compared to IFA; (ii) induce toxicity compared to ALU or (iii) elicit anti-RNP/Sm autoantibody, as occurred in the CFA group.

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“…Levels of IgG ANA were sought by indirect immunofluorescence using Hep-2 cells. Anti-dsDNA Abs were detected by indirect immunofluorescence on Crithidia luciliae (12). Serum samples were screened at a 1/80 (ANA) or a 1/20 (anti-dsDNA) dilution, and the positive samples were titrated to end point.…”

Section: Autoantibody Assaysmentioning

confidence: 99%

C1q Deficiency and Autoimmunity: The Effects of Genetic Background on Disease Expression

Mitchell

Pickering

Warren

et al. 2002

The Journal of Immunology

210

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Gene-targeted C1q-deficient mice have been shown to develop a syndrome reminiscent of human systemic lupus erythematosus with antinuclear Abs and proliferative glomerulonephritis. Initial phenotypic analysis conducted in (129 × C57BL/6) hybrid mice showed that background genes were a significant factor for the full expression of the autoimmune disease. To assess the contribution of background genes in the expression of the autoimmune phenotype, the disrupted C1qa gene was backcrossed for seven generations onto C57BL/6 and MRL/Mp+/+ strains. These were intercrossed with C57BL/6.lpr/lpr and MRL/Mp-lpr/lpr strains to generate C1q-deficient substrains. In C1q-deficient C57BL/6 mice, no evidence of an autoimmune phenotype was found, and C1q deficiency in both the C57BL/6.lpr/lpr and MRL/Mp-lpr/lpr strains did not modify the autoimmune phenotype observed in wild-type controls. However, in C1q-deficient MRL/Mp+/+ animals an acceleration of both the onset and the severity of antinuclear Abs and glomerulonephritis was seen. Disease was particularly pronounced in females, which developed severe crescentic glomerulonephritis accompanied by heavy proteinuria. In addition, the C1q-deficient MRL/Mp+/+ mice had an impairment in the phagocytic clearance of apoptotic cells in vivo. These data demonstrate that the expression of autoimmunity in C1q-deficient mice is strongly influenced by other background genes. The work also highlights the potential value of the C1q-deficient MRL/Mp+/+ strain as a tool with which to dissect further the underlying mechanisms of the autoimmune syndrome associated with C1q deficiency.

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Measurement of anti-DNA antibodies: a reappraisal using five different methods.

Cited by 103 publications

References 26 publications

Measurement of increases in anti‐double‐stranded dna antibody levels as a predictor of disease exacerbation in systemic lupus erythematosus

Measurement of increases in anti‐double‐stranded dna antibody levels as a predictor of disease exacerbation in systemic lupus erythematosus

Effects of adjuvants for human use in systemic lupus erythematosus (SLE)-prone (New Zealand black/New Zealand white) F1 mice

C1q Deficiency and Autoimmunity: The Effects of Genetic Background on Disease Expression

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