Anti-Dna Antibodies in the Primary Antiphospholipid Syndrome (Paps)

Ehrenstein, Michael R.; Swana, M.; Keeling, David; Ra, Asherson; Hughes, G. R. V.; Isenberg, David

doi:10.1093/rheumatology/32.5.362

Cited by 26 publications

(12 citation statements)

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“…As discussed above about plasma levels of sRAGE, there was no good explanation for such findings. Although not often examined in pAPS patients, some studies indicated that the production of autoantibodies is prevalent in pAPS patients [31,32]. Interestingly, we observed a poor correlation between plasma levels of HMGB1 measured by ELISA and Western blot.…”

Section: Discussioncontrasting

confidence: 68%

Plasma levels of high-mobility group box 1 and soluble receptor for advanced glycation end products in primary antiphospholipid antibody syndrome patients

et al. 2017

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IntroductionMany studies have demonstrated elevated circulating levels of high-mobility group box 1 (HMGB1) and decreased circulating levels of soluble receptor for advanced glycation end products (sRAGE) in patients with autoimmune diseases. In the present study, we investigated plasma levels of both HMGB1 and sRAGE in primary antiphospholipid syndrome (pAPS) patients.MethodsWe prospectively recruited 11 pAPS patients, 17 antiphospholipid antibody (APA)-positive SLE patients without APS manifestations (APA+SLE) and 12 SLE patients with secondary APS (APS+SLE). We also recruited 10 healthy controls (HCs). Plasma levels of HMGB1 and sRAGE were determined using sandwich ELISA kits. In addition, plasma levels of HMGB1 were also determined using Western blot in 6 pAPS patients and 6 HCs.ResultsThere was no significant difference in plasma levels of HMGB1 measured by ELISA among subgroups of the enrolled subjects. In addition, there was no significant difference in plasma levels of HMGB1 measured by Western blot between pAPS patients and HCs. On the other hand, we observed a trend toward lower plasma levels of sRAGE in APA+SLE or APS+SLE patients when compared with HCs. However, there was no significant difference in plasma levels of sRAGE between pAPS patients and HCs, or between APA+SLE patients and APS+SLE patients.ConclusionThere was no significant difference in plasma levels of sRAGE or HMGB1 between pAPS patients and HCs. Plasma levels of sRAGE/HMGB1 could not be utilized to differentiate between APA+SLE and APS+SLE patients.

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Section: Discussioncontrasting

confidence: 68%

Plasma levels of high-mobility group box 1 and soluble receptor for advanced glycation end products in primary antiphospholipid antibody syndrome patients

et al. 2017

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“…To coat dsDNA, calf thymus dsDNA was adsorbed to a 96-well ELISA plate precoated with poly- l -lysine (50 μg/ml) at 4°C overnight [41]. After charge neutralizing the plates with poly- l -glutamate (100 μg/ml in distilled water), the plates were blocked with 2% casein (37°C, 1 h for each step).…”

Section: Methodsmentioning

confidence: 99%

Specific cross-reaction of anti-dsDNA antibody with platelet integrin GPIIIa49-66

Zhang¹,

Dang²,

Wang³

et al. 2010

Autoimmunity

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Anti-platelet autoantibodies are frequently found in systemic lupus erythematosus (SLE) patients and contribute to the development of SLE-associated immunologic thrombocytopenia (SLE-ITP). Although the correlation of anti-dsDNA autoantibody with platelet-associated antibody has been reported, the potential mechanism underlying such a correlation is incompletely understood. We have reported that anti-platelet integrin GPIIIa49-66 (CAPESIEFPVSEARVLED) autoantibodies play a major role in the development of HIV-1-related thrombocytopenia (HIV-1-ITP). The strong negative charge of GPIIIa49-66 prompts us to investigate whether GPIIIa49-66 can be an epitope mimicking dsDNA. We report here that anti-GPIIIa49-66 antibodies are found in three out of nine SLE-ITP patients. Double-stranded (ds) DNA competitively inhibited the binding of purified patient anti-dsDNA antibodies to GPIIIa49-66 peptide. Both polyclonal and monoclonal anti-GPIIIa49-66 antibodies are able to cross-react with dsDNA. Consistent with previous reports, the DNA binding activities of anti-GPIIIa49-66 antibodies are mainly dependent on the positively charged amino acid in the heavy-chain complementarity-determining region 3 (HCDR3). The HCDR3 of human SLE anti-dsDNA monoclonal antibody (mAb) 412.67 demonstrates a similar positively charged amino acid chain orientation compared with that of anti-GPIIIa49-66 mAb A11, and it cross-reacts with GPIIIa49-66 peptide. Purified anti-GPIIIa49-66 antibodies from SLE-ITP patients are able to induce platelet fragmentation in vitro and to induce thrombocytopenia in vivo. Thus, our data suggest that specific epitope cross-reaction between GPIIIa49-66 and dsDNA could be a mechanism involved in the development of SLE-associated thrombocytopenia.

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“…Anti‐DNA antibodies have been reported in patients with a variety of rheumatologic diseases and other conditions including: rheumatoid arthritis, Sjögren's syndrome, scleroderma, drug induced lupus, Raynaud's phenomenon, mixed connective tissue disease, discoid lupus, myositis, chronic active hepatitis, other liver diseases, uveitis, relatives of SLE patients, patients hospitalized for nonrheumatologic diseases, Graves' disease, Alzheimer's disease, juvenile rheumatoid arthritis, certain laboratory workers, anticardiolipin antibody syndrome, and persons with silicone breast implants (41–60). The frequency of elevated levels of anti‐DNA antibodies in conditions other than SLE is uniformly low (≤5% of patients), and when present, they are often present in low titer.…”

Section: Indications For Clinical Use Of the Anti‐dna Antibody Testmentioning

confidence: 99%

Guidelines for immunologic laboratory testing in the rheumatic diseases: Anti‐DNA antibody tests

Kavanaugh

Solomon

2002

Arthritis & Rheumatism

197

119

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This paper is part of a series on immunologic testing guidelines. The series introduction (1) outlines the full methodology for obtaining data, grading the literature, combining the information from multiple sources, and developing recommendations. Briefly, MEDLINE and Healthstar were searched using a variety of search terms, and all relevant available literature was reviewed. All papers were critically reviewed using published standards for studies of diagnostic tests. Test use was categorized as primarily diagnostic or prognostic (which also included monitoring). Information was extracted from each paper to allow for calculation of a weighted average for sensitivity and specificity; likelihood ratios (LRs) were then derived from these values (positive LR ϭ sensitivity/[1 Ϫ specificity]; negative LR ϭ [1 Ϫ sensitivity]/specificity). Recommendations for use of tests were based on the LRs, where a test was considered to be "very useful" for a given disease if the weighted average positive LR was Ͼ5 or negative LR was Ͻ0.2. A test was considered "useful" if the weighted average positive LR was Ͼ2 and Յ5 or negative LR was Ͼ0.2 and Յ0.5. A test was considered "not useful" if the positive LR was Յ2 or the negative LR was Ͼ0.5.Antibodies capable of binding double-stranded DNA (dsDNA), single-stranded DNA (ssDNA), Z-DNA, and various other proteins associated with DNA (e.g., histones) can be detected in the serum of patients with systemic lupus erythematosus (SLE). In this analysis, the term anti-DNA antibody will refer only to antibodies specific for dsDNA (also referred to as native DNA). A number of studies have shown that antibodies to ssDNA (also referred to as denatured DNA) are less specific for the diagnosis of SLE than anti-dsDNA antibodies. While anti-ssDNA antibodies may be a useful research tool, they are an infrequently used clinical test, and will not be addressed further in this analysis.

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Anti-Dna Antibodies in the Primary Antiphospholipid Syndrome (Paps)

Cited by 26 publications

References 0 publications

Plasma levels of high-mobility group box 1 and soluble receptor for advanced glycation end products in primary antiphospholipid antibody syndrome patients

Plasma levels of high-mobility group box 1 and soluble receptor for advanced glycation end products in primary antiphospholipid antibody syndrome patients

Specific cross-reaction of anti-dsDNA antibody with platelet integrin GPIIIa49-66

Guidelines for immunologic laboratory testing in the rheumatic diseases: Anti‐DNA antibody tests

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