Self-dsDNA in the pathogenesis of systemic lupus erythematosus.
Y BaiY TongY LiuHongbo HuPublished in: Clinical and experimental immunology (2017)
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.
Keyphrases
- systemic lupus erythematosus
- disease activity
- circulating tumor
- cell free
- single molecule
- end stage renal disease
- ejection fraction
- dendritic cells
- cell death
- oxidative stress
- immune response
- newly diagnosed
- nucleic acid
- gene expression
- multiple sclerosis
- bone marrow
- stem cells
- prognostic factors
- transcription factor
- risk assessment
- dna methylation
- anti inflammatory
- binding protein
- climate change
- human health