Anti-dsDNA (Mouse) IgG ELISA Kit

Systemic lupus erythematosus (SLE) is a severe autoimmune disease that produces various antibodies and involves multiple organs. Since 1982, anti-double-stranded DNA (anti-dsDNA) antibodies have been listed as diagnostic criteria for SLE by the American College of Rheumatology (ACR), and studies have noted a high correlation between anti-dsDNA antibodies and lupus nephritis (LN). Furthermore, anti-dsDNA antibodies are relatively effective indicators for monitoring SLE disease activity. Nuclear substances originate from billions of dead cells daily due to senescence, infections, or mechanical injuries. Normally, the immune system is not accessible to nuclear antigens because dead cells are quickly cleared to achieve self-stability, avoiding the accumulation of nuclear antigens. Dysregulation of various cell death processes (e.g., apoptosis, necrosis, NETosis, and autophagy) accounts for the exposure of nuclear autoantigens. Dysregulation of dead cells and clearance deficiency have been suggested in Systemic lupus erythematosus (SLE) patients. Anti-dsDNA antibodies can recognize released dsDNA and compose ICs. In SLE patients, TLRs, especially TLR7 and TLR9, are crucial in the loss of B cell tolerance. They recognize BCR-mediated internalized self-nucleic acids. The discrepancy of the anti-dsDNA antibody subclass (IgM, IgG1, IgG2a, IgG2b, and IgG3) has a remarkably different affinity and pathogenicity in SLE.

Figure 1. The pathogenic mechanism of anti-dsDNA antibodies in neuropsychiatric lupus, lupus nephritis, and CLE.
(Source: Yaqi Wang. et al., 2022)

Anti-dsDNA antibody, the hallmark of SLE, contributes to kidney, brain, and skin damage in SLE. The pathogenicity of autoantibodies had been used to develop a means of attempts to reduce anti-dsDNA antibodies, including immunosuppression, immunoadsorption, B cell-targeting, and iDC vaccine therapies. However, immunosuppression and B cell-targeting therapies are not distinctive for lupus and may hamper normal immune system functioning, which bring unavoidable adverse effects. Notably, the mimic peptides designed by blocking anti-dsDNA antibodies highlight the promising therapeutic potential to ameliorate the manifestation of SLE. The peptides' small molecular property demonstrates advances in high-throughput and standardized and modified synthesis technology. However, most of the peptides are now at the preclinical stage and have a short half-life and unsatisfactory physiological stability. Further studies are warranted to develop more effective therapies for SLE.

Current methodologies for detecting anti-dsDNA antibodies include Farr radioimmunoassay, Crithidia luciliae indirect immunofluorescence test (CLIFT), enzyme-linked immunosorbent assay (ELISA), fluoroenzyme immunoassay (FEIA), and chemiluminescent immunoassay (CIA). Although the Farr radioimmunoassay has high sensitivity and specificity, it is rarely used clinically due to its use of radioactive materials. CLIFT involves using the kinetoplast of Crithidia luciliae to form a specific combination with anti-dsDNA antibodies, making it highly specific. However, its sensitivity is lower than that of other methods, particularly in detecting early SLE, rendering it unsuitable as a screening test. Moreover, CLIFT is limited by qualitative inspections, requires manual interpretation, and is prone to differences due to microscope equipment, making it difficult to be used as a method for disease activity monitoring. Therefore, ELISA and CIA are preferred for clinical monitoring of disease activity.