Journal
CLINICAL AND EXPERIMENTAL IMMUNOLOGY
Volume 191, Issue 1, Pages 1-10Publisher
WILEY
DOI: 10.1111/cei.13041
Keywords
autoantibody; DNA sensors; IFN-I; self-dsDNA; SLE
Categories
Funding
- Ministry of Science and Technology (the National Key Research and Development Program) [2016YFA0502203, 2016YFC0906201]
- Ministry of Science and Technology (Recruitment Program of Global Experts)
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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.
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