Detection of Antibodies to dsDNA: An Overview of Laboratory Assays

Lupus ◽  
2006 ◽  
Vol 15 (7) ◽  
pp. 403-407 ◽  
Author(s):  
AM Rouquette ◽  
C Desgruelles
Keyword(s):  
Antibodies To Dsdna

scholarly journals Low avidity antibodies to dsDNA as a diagnostic tool.

1989 ◽  
Vol 48 (9) ◽  
pp. 748-752 ◽  
Author(s):  
J C Nossent ◽  
V Huysen ◽  
R J Smeenk ◽  
A J Swaak
Keyword(s):  
Diagnostic Tool ◽  
Antibodies To Dsdna

scholarly journals Reevaluation of enzyme-linked immunosorbent assay with ultraviolet-treated polystyrene microtiter plates for measurement of antibodies to dsDNA.

1996 ◽  
Vol 19 (2) ◽  
pp. 163-167
Author(s):  
Junichi Kaburaki ◽  
Takashi Ogasawara ◽  
Masakatsu Hayakawa ◽  
Masataka Kuwana ◽  
Takeshi Tojo ◽  
...  
Keyword(s):  
Immunosorbent Assay ◽  
Enzyme Linked Immunosorbent Assay ◽  
Microtiter Plates ◽  
Antibodies To Dsdna

Prevention and Reversal of Lupus in NZB/NZW Mice by Transplantation of Purified Allogeneic Hematopoietic Stem Cells (HSC) with Non-Myeloablative Conditioning (NMT).

Blood ◽  
2006 ◽  
Vol 108 (11) ◽  
pp. 3198-3198
Author(s):  
Stephanie Smith-Berdan ◽  
Daphne Gille ◽  
Julie L. Christensen
Keyword(s):  
Lupus Erythematosus ◽  
Matched Control ◽  
Mixed Chimerism ◽  
Final Time ◽  
Myeloablative Conditioning ◽  
Hematopoietic Stem ◽  
Living Well ◽  
Nuclear Antigens ◽  
Final Time Point ◽  
Antibodies To Dsdna

Abstract Systemic lupus erythematosus (SLE) is a multifactorial autoimmune disease. Patients’ refractory to therapy may be considered for hematopoietic stem cell transplantation. Using lupus prone female NZB x NZW (NZBW) mice, we tested the ability of highly enriched, allogeneic HSC to prevent and reverse autoimmune symptoms with FACS purified haplo-identical allogeneic HSC. Ablative conditioning: 92 animals were given lethal TBI (14.5 Gy) and divided among 4 groups (Table 1). Urine and serology tested monthly, final time point before death tabulated. Transplantation with either syngeneic HSC or WBM accelerated disease in these mice, resulting in a rate of death exceeding age matched controls. Allogeneic transplanted mice had significantly greater survival above all groups (p= 0.0243). Proteinuria, elevated levels of circulating immune complexes (CIC), and auto-antibodies to dsDNA, nuclear antigens (ANA) and histones were lower in allo-HSC animals compared to the other ablative conditioning groups (p≤ 0.0001). Overall survival (OS) in allo-HSC animals was still unexceptional, possibly due to regimen related toxicity (TRM). Table 1: Ablative age@TX=75 days Age Matched Control Syngeneic WBM Syngeneic HSC Allogeneic HSC N 15 21 28 28 OS@420 days of age 20% 0% 0% 53% Proteinuria 100% 74% 75% 15% CIC 93% 81% 100% 25% Anti-dsDNA 100% 91% 100% 39% Anti-ANA 100% 86% 93% 39% Anti-Histone 93% 91% 100% 46% NMT conditioning: To determine if we could attenuate disease in NZBW mice already progressing into lupus-like disease with transplantation of allogeneic, purified HSC and reduce TRM, we developed a non-myeloablative conditioning protocol (2x5 Gy TBI + ATG + a-ASIALO-GM1) achieving an average mixed chimerism of 50%. Animals were treated at ~241 days with established symptoms of lupus (Table 2). While the group receiving conditioning alone, had a slight survival advantage over age matched control mice, the transplanted mice had greatly increased OS with 70% living well beyond 500 days of age (>250 days from transplant). Allo-HSC mice showed reversal or stabilization of their lupus symptoms including proteinuria, CIC, dsDNA and histone. Table 2: NMT age@Tx=241 days Age Matched Control Allogeneic HSC Conditioned Only N 10 33 30 OS@500 days of age 0% 70% 0% Proteinuria@Tx 20% 49% 47% Final Proteinuria 100% 39% 67% CIC 67% 50% 74% Anti-dsDNA 85% 15% 44% Anti-Histone 100% 37% 66% Conclusions: Ablative and NMT transplant can treat lupus; OS after NMT exceeds ablative conditioning; Induction of mixed chimerism with purified allogeneic HSC using NMT conditioning treats established lupus. The ability of pure HSC transplant and establishment of durable mixed chimerism to reverse established lupus makes it a reasonable strategy to test in man.

Relationship Between Antibodies to Dsdna and to Soluble Cellular Antigens and Histologically Defined Glomerulonephritis in Patients with SLE

Autoimmunity ◽  
1990 ◽  
Vol 7 (1) ◽  
pp. 13-21 ◽  
Author(s):  
R. Asero ◽  
G. Banfi ◽  
L. Radelli ◽  
L. Origgi ◽  
E. Bertetti ◽  
...  
Keyword(s):  
Antibodies To Dsdna

Value of a commercial kit for detecting anti-C1q autoantibodies and correlation with immunological and clinical activity of lupus nephritis

2015 ◽  
Vol 53 (11) ◽  
Author(s):  
Federica de Liso ◽  
Caterina Matinato ◽  
Cristina Novembrino ◽  
Antonella Radice ◽  
Francesca Raffiotta ◽  
...  
Keyword(s):  
Lupus Nephritis ◽  
Blood Cells ◽  
Renal Involvement ◽  
Roc Curves ◽  
Clinical Activity ◽  
Serum Samples ◽  
Contingency Coefficient ◽  
Antibodies To Dsdna ◽  
Commercial Kit

AbstractThe association of anti-C1q antibodies (anti-C1q) with the renal activity of lupus nephritis (LN) and the methods for their determination is still a matter of debate.In 116 serum samples of 66 patients with biopsy proven LN, we aimed: 1) to compare the results of the determination of anti-C1q obtained by a commercial kit with a clinically validated in-house ELISA; 2) to evaluate the correlation of anti-C1q with the most important immunological and clinical parameters employed in LN, i.e., antibodies to dsDNA (anti-dsDNA), C3 and C4 complement component, haemoglobin and haematuria.Good correlation and agreement between the two methods (r=0.81, p<0.0001; contingency coefficient=0.70, p<0.0001, respectively) were demonstrated. No differences were observed between the two assays by ROC curves comparison. Anti-C1q levels were significantly higher in patients with active LN [44 arbitrary units (AUs)] in comparison to those with inactive LN (23 AUs, p=0.047) and significantly correlated with anti-dsDNA (r=0.44, p<0.0001), complement fractions (C3: r=−0.33, p=0.001; C4: r=−0.29, p=0.003), haemoglobin levels (r=−0.34, p=0.0004) and the number of urinary red blood cells (r=0.26, p=0.01).Our results suggest the validity of this commercial assay in detecting anti-C1q and confirm the association of anti-C1q with renal involvement of LN and the importance of introducing this parameter in the analytical panel for the evaluation of LN activity.

scholarly journals Neutralizing anti-DNase1L3 antibodies derive from autoreactive VH4-34+ B cells and associate with the interferon signature in SLE

2021 ◽  
Author(s):  
Felipe Andrade ◽  
Yikai Yu ◽  
Eduardo Gomez-Banuelos ◽  
Jessica Li ◽  
Kevin S. Cashman ◽  
...  
Keyword(s):  
B Cells ◽  
Lupus Erythematosus ◽  
Inborn Error ◽  
Gene Segment ◽  
Memory B Cells ◽  
Chain Gene ◽  
Heavy Chain Gene ◽  
Interferon Signature ◽  
Immune Pathways ◽  
Antibodies To Dsdna

DNase1L3 deficiency is an inborn error of immunity that causes monogenic systemic lupus erythematosus (SLE) in humans. Here, we identified that one third of patients with sporadic SLE have antibodies to DNase1L3. Like DNase1L3 deficiency, we found that patients with anti-DNase1L3 antibodies have features associated with immune pathways activated by immunogenic self-DNA, including elevated antibodies to dsDNA and prominent expression of the interferon and myeloid/neutrophil signatures. Interestingly, 40-80% of anti-DNase1L3 antibodies in SLE serum contain the 9G4 idiotype, which is encoded by the autoreactive heavy-chain gene segment VH4-34. Sequence and functional analysis of four anti-DNase1L3 monoclonal antibodies generated from SLE patients experiencing disease-associated flares showed that these antibodies were derived from self-reactive 9G4+ switched memory B cells. These antibodies are highly enriched in somatic hypermutations, indicating that they originated from antigen-experienced cells, and have neutralizing activity against DNase1L3. Together, the data demonstrate that autoantibodies to DNase1L3 phenocopy pathogenic mechanisms associated with DNase1L3 deficiency. Moreover, the finding that autoreactive B cells bearing the 9G4 idiotype produce dominant serum autoantibodies, including antibodies to DNase1L3, underscores VH4-34+ B cells as sensible therapeutic targets for specific depletion of pathogenic B cells in SLE.

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