Self‐dsDNA in the pathogenesis of systemic lupus erythematosus

Summary Systemic lupus erythematosus (SLE) is a systemic and poly‐aetiological autoimmune disease characterized by the production of antibodies to autologous double‐stranded DNA (dsDNA) which serve as diagnostic and prognostic markers. The defective clearance of apoptotic material, together with neutrophil extracellular traps (NETs), provides abundant chromatin or self‐dsDNA to trigger the production of anti‐dsDNA antibodies, although the mechanisms remain to be elucidated. In SLE patients, the immune complex (IC) of dsDNA and its autoantibodies trigger the robust type I interferon (IFN‐I) production through intracellular DNA sensors, which drives the adaptive immune system to break down self‐tolerance. In this review, we will discuss the potential resources of self‐dsDNA, the mechanisms of self‐dsDNA‐mediated inflammation through various DNA sensors and its functions in SLE pathogenesis. In this review, we discussed potential resources of self‐dsDNA, the mechanisms of self‐dsDNA mediated inflammation through various DNA sensors, and its functions in SLE pathogenesis.