Serum Immune Complexes and Disease Activity in Lupus Nephritis

Levinsky, R J; Cameron, J. S.; Soothill, J. F.

doi:10.1016/s0140-6736(77)91998-5

Cited by 142 publications

(47 citation statements)

References 6 publications

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“…Immune complex measurement in SLE by other assays have had variable results. Concordance of disease activity and IC levels has been reported for the Clq deviation test (13) and the polyclonal latex agglutination inhibition test (14), while the lymphocyte rosette inhibition assay correlated poorly with activity (15). The Raji cell assay and the monoclonal rheumatoid factor assay (16) showed concordance with nonrenal disease but not with renal disease.…”

Section: Discussionmentioning

confidence: 91%

The C1q binding assay in systemic lupus erythematosus

Inman

Fong

Pussell

et al. 1980

Arthritis & Rheumatism

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To investigate the relationship of Clq binding assay (ClqBA) to disease activity in systemic lupus erythematosus (SLE), a retrospective study was carried out on 232 ClqBA performed in 33 patients with SLE.When initial values only were assessed (33 tests in 33 patients), there was no relationship between positive and negative ClqBA and abnormal renal function (P = 0.482, Fisher exact test). Of 87 tests performed during active renal disease, 34 (39%) were positive; of 48 tests during active non-renal disease, 25 (52%) were positive; of 83 tests when the disease was inactive, 45 (54%) were positive; and of 14 tests during episodes of infection, 10 (71%) were positive. Corresponding means for the ClqBA were as follows: renal 65.66, non-renal78.02, inactive 56.04, infection 135.79 (no significant diarerences by Student's f-test). There was no significant relationship with the ClqBA when comparing active disease (renal and non-renal) with inactive disease ($ Yates = 1.875, P = 0.171). When renal function abnormalities were analyzed separately, the ClqBA values were inde-

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Section: Discussionmentioning

confidence: 91%

The C1q binding assay in systemic lupus erythematosus

Inman

Fong

Pussell

et al. 1980

Arthritis & Rheumatism

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“…The demonstration of anti-DNA antibodies in pathologic tissues, the correlation between their levels in serum and disease activity, and their high prevalence, suggest that anti-DNA antibodies participate in the pathogenesis of SLE [1,2]. Tissue deposition of DNA-anti-DNA immune complexes has been regarded as a prerequisite in disease pathogenesis [3,4]. However, it remains doubtful whether this represents the predominant pathogenic mechanism, in view ofthe inconsistent detection of circulating immune complexes, and the failure to produce similar pathologies upon injection of pre-formed immune complexes in animal experiments [5,6].…”

Section: Introductionmentioning

confidence: 99%

Endothelial cell binding by human polyclonal anti-DNA antibodies: relationship to disease activity and endothelial functional alterations

Chan

Tsang

et al. 1995

Clinical and Experimental Immunology

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SUMMARY Polyclonal anti‐dsDNA and anti‐ssDNA antibodies (PoAb) that showed significant binding to human umbilical vein endothelial cells (HUVEC) were isolated from eight patients with systemic lupus erythematosus (SLE). Anti‐dsDNA PoAbs from five patients and anti‐ssDNA PoAbs from seven patients demonstrated enhanced binding to HUVEC during active disease, compared with PoAbs obtained from corresponding patients during remission. Reduction of the DNA content in the PoAb preparations by DNase treatment was associated with enhanced binding to HUVEC in 20 of 32 PoAbs tested, which included 75%‘active disease’ PoAbs, and with reduced binding to HUVEC in three of 32 PoAbs tested, all obtained during remission. Such altered endothelial cell binding was reversed with DNA reconstitution. Binding of the remaining nine PoAbs to HUVEC was not altered by variations in their DNA content. Induced plasma membrane expression of E‐selectin, but reduced expression of vascular cell adhesion molecule‐1 (VCAM‐1) by HUVEC, was observed following incubation of HUVEC with ‘active disease’ PoAbs from three and two of the eight patients, respectively. PoAbs and serum samples from two of the eight patients during active disease induced von Willebrand factor release from HUVEC, which was not observed during remission. We conclude that anti‐DNA antibodies from selected patients with SLE can bind to endothelial cells. Correlation between cellular binding and disease activity suggests that such binding of anti‐DNA antibodies to endothelial cells could be of pathogenic significance. Preliminary data also suggest that the expression of adhesion molecules and haemostatic factor(s) by endothelial cells may be modified following their binding by anti‐DNA antibodies.

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“…Others have reported the sedimentation coeffi cients of CIC to vary from 13 S to 19 S [15,16,23], but the methods used only allowed measurements of CIC below 19 S [15.16], Levinsky ct al. [12] have reported that in patients with SLE nephritis without extrarenal signs the MW of the CIC was 1-1.5 x |0 8, and in those with the MW was 2.5-4 x 10". In agreement with this, CIC with MW above 1.2 x 10" were only detected in patients with extrarenal manifesta tions.…”

Section: W O F Cic In Glomerulonephritismentioning

confidence: 97%

Molecular Weight of Circulating Immune Complexes in Patients with Glomerulonephritis

Sølling¹

1982

Nephron

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The C1q-binding test was used to detect circulating immune complexes in 86 patients with glomerulonephritis at the time of renal biopsy. By gel filtration of the sera it was possible to estimate the molecular weight in 24 of these patients. The molecular weight ofcirculating immune complexes varied from 150,000 to above 1.2 × 10⁶ and was not related to the type of glomerulonephritis as defined by light microscopy, renal function, proteinuria, hematuria or antecedent infections. In 8 patients with rheumatoid arthritis and in 5 patients with secondary syphilis and no evidence of renal disease, only circulating immune complexes with a molecular weight below 1.2 × 106 were detected. 7 patients with glomerulonephritis had electron-dense deposits in glomeruli on electron microscopy, but the molecular weight ofcirculating immune complexes was not related to the site of the deposits on either side of the basement membrane.

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Serum Immune Complexes and Disease Activity in Lupus Nephritis

Cited by 142 publications

References 6 publications

The C1q binding assay in systemic lupus erythematosus

The C1q binding assay in systemic lupus erythematosus

Endothelial cell binding by human polyclonal anti-DNA antibodies: relationship to disease activity and endothelial functional alterations

Molecular Weight of Circulating Immune Complexes in Patients with Glomerulonephritis

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