Anti dsDNA antibody in systemic lupus erythematosus

Systemic lupus erythematosus (SLE) is a complex autoimmune disease characterized by dysregulated immune responses against self-antigens, resulting in chronic inflammation and tissue damage. Among the diverse array of autoantibodies detected in SLE patients, anti-double-stranded DNA (anti-dsDNA) antibodies hold particular clinical significance due to their association with disease activity, organ damage, and prognosis.


Immunopathogenesis of systemic lupus erythematosus. Autoantibodies form immune complexes with circulating autoantigens. Complement binds to autoantibody–antigen complexes and deposits in tissues to trigger inflammatory responses


Anti-dsDNA antibodies specifically target double-stranded DNA molecules, forming immune complexes that deposit in tissues and trigger inflammatory responses, particularly in the kidneys. The presence of anti-dsDNA antibodies has been strongly correlated with lupus nephritis, a severe manifestation of SLE characterized by renal inflammation and dysfunction. Detection of anti-dsDNA antibodies is thus considered a valuable diagnostic marker for lupus nephritis and helps guide treatment decisions.

Furthermore, anti-dsDNA antibodies have been implicated in the pathogenesis of SLE through various mechanisms. These antibodies can directly bind to cell surface receptors, such as Toll-like receptors (TLRs), leading to the activation of innate immune responses and production of pro-inflammatory cytokines. Additionally, immune complexes formed by anti-dsDNA antibodies can activate the complement system, resulting in tissue inflammation and damage.

In clinical practice, monitoring anti-dsDNA antibody levels serves as an essential tool for assessing disease activity and guiding therapeutic interventions in SLE patients. Elevated levels of anti-dsDNA antibodies often correlate with disease flares, prompting intensification of immunosuppressive therapy to control inflammation and prevent organ damage. Conversely, declining anti-dsDNA antibody titers may indicate treatment response and disease remission.

Despite their clinical relevance, the specificity and sensitivity of anti-dsDNA antibody assays vary, posing challenges in their accurate detection and interpretation. Therefore, a comprehensive approach that incorporates clinical assessment, serological testing, and monitoring of disease activity is essential for effectively managing SLE patients.

Autoantibodies in SLE:

SLE is characterized by the production of a wide array of autoantibodies, which are antibodies that target the body's own tissues and antigens. These autoantibodies contribute to the autoimmune response and tissue damage observed in SLE. Besides anti-dsDNA antibodies, other common autoantibodies in SLE include anti-nuclear antibodies (ANAs), anti-Smith (Sm) antibodies, anti-Ro (SSA) and anti-La (SSB) antibodies, and anti-phospholipid antibodies.

Production of Anti-dsDNA Antibodies:

Anti-dsDNA antibodies are produced by B lymphocytes, a type of white blood cell, in response to the presence of double-stranded DNA (dsDNA) molecules. The exact triggers for the production of these antibodies in SLE are not fully understood but are believed to involve a combination of genetic predisposition, environmental factors, and dysregulation of the immune system.

Role in Tissue Damage:

Anti-dsDNA antibodies play a central role in the pathogenesis of SLE by forming immune complexes with dsDNA molecules. These immune complexes can deposit in various tissues, including the kidneys, skin, joints, and blood vessels. In particular, deposition of immune complexes in the kidneys can lead to lupus nephritis, a severe and potentially life-threatening complication of SLE characterized by inflammation and damage to the renal tissue.

Inflammatory Responses:

Upon deposition in tissues, immune complexes containing anti-dsDNA antibodies can trigger inflammatory responses. This can involve the recruitment and activation of immune cells, such as neutrophils and macrophages, leading to local inflammation and tissue damage. Additionally, anti-dsDNA antibodies may directly activate complement proteins, further amplifying the inflammatory cascade.

Association with Disease Activity:

Levels of anti-dsDNA antibodies often fluctuate with disease activity in SLE patients. High levels of anti-dsDNA antibodies are frequently observed during disease flares, correlating with increased disease activity and severity. Conversely, declining levels of anti-dsDNA antibodies may coincide with disease remission or response to treatment.

Diagnostic and Prognostic Marker:

Detection of anti-dsDNA antibodies is an important component of the diagnostic workup for SLE, particularly in patients with lupus nephritis. Additionally, anti-dsDNA antibody levels may serve as a prognostic marker for disease progression and organ involvement, helping to guide treatment decisions and monitor response to therapy.

Systemic lupus erythematosus (SLE) is a complex autoimmune disease characterized by the production of a wide range of autoantibodies and dysfunctional activation of the complement system. The specific association between complement component C3a (C3a) protein and antibodies specific for double-stranded DNA (anti-dsDNA), however, has not been studied in detail to date.

This study was therefore designed to further explore the circulating levels of C3a in patients with SLE. A total of 13 patients with SLE were included in this study after being diagnosed according to the SLICC classification criteria, with 7 and 6 patients showing positivity for anti-dsDNA and anti-Sm autoantibodies, respectively. Levels of serum complement components C1q (C1q) and C3a in samples from these patients were detected by Western blot, while other serological, biochemical, and clinical parkers associated with disease activity were detected by Western blot. using standard laboratory techniques.

Serum C3a levels in anti-dsDNA+  patients were significantly elevated compared to those in anti-Sm+  patients (P <0.01), and a positive correlation between serum C3a levels and the index scores of SLE disease activity was detected (P<0.05, r=0.6134). C3a levels are correlated with the degree of SLE disease activity and other clinically relevant readings in patients with SLE. C3a levels may also allow differentiation between inactive and active SLE, while also providing value as a beneficial biomarker for monitoring thrombophilia in patients with SLE.

The complement system is an evolutionarily ancient facet of the innate immune system that plays a critical role in protecting the host against many potential pathogens1. Different stimuli can induce complement activation through three different pathways, ultimately resulting in a common response conducive to clearing infection and restoring immune homeostasis2,3. Anaphylatoxin small subunits of complement proteins C3 and C5 (C3a and C5a) are important drivers of inflammatory responses, promoting mast cell degranulation, smooth muscle contraction, improved vascular permeability, chemotaxis immune cells and the release of pro-inflammatory cytokines4. While complement is beneficial when activated appropriately, its dysfunctional or inappropriate activation can contribute to a loss of host homeostasis that can facilitate infection, autoimmunity, oncogenic progression, and /or tissue damage2.

Systemic lupus erythematosus (SLE) is a persistent and debilitating autoimmune disease that primarily affects women and can occur in people of any age, gender or ethnicity5. Patients with SLE typically exhibit a wide array of autoantibodies and complement system dysfunction that may contribute to the incidence of tissue and organ damage6. The most common autoantibodies specific to SLE patients are those specific for Smith (Sm) and double-stranded DNA (dsDNA), with the presence of one or more of these autoantibodies being important for the classification of SLE disease7. Anti-dsDNA levels often vary over time in SLE patients and may even resolve in some cases with appropriate treatment8. Anti-Sm antibody levels, on the other hand, tend to be stable and resistant to treatment-related changes