Anti dsDNA antibody in systemic lupus erythematosus
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