The role of neutrophil extracellular traps and proinflammatory damage-associated molecular patterns in idiopathic inflammatory myopathies.
Wenlan MaJiarui ZhuLing BaiPeipei ZhaoFeifei LiSigong ZhangPublished in: Clinical and experimental immunology (2023)
Idiopathic inflammatory myopathies (IIMs) are a group of systemic autoimmune diseases characterized by immune-mediated muscle injury. Abnormal neutrophil extracellular traps (NETs) can be used as a biomarker of IIM disease activity, but the mechanism of NET involvement in IIMs needs to be elucidated. Important components of NETs, including high-mobility group box 1 (HMGB1), DNA, histones, extracellular matrix (ECM), serum amyloid A (SAA), and S100A8/A9, act as damage-associated molecular patterns (DAMPs) to promote inflammation in IIMs. NETs can act on different cells to release large amounts of cytokines and activate the inflammasome, which can subsequently aggravate the inflammatory response. Based on the idea that NETs may be proinflammatory DAMPs of IIMs, we describe the role of NETs, DAMPs, and their interaction in the pathogenesis of IIMs and discuss the possible targeted treatment strategies in IIMs.
Keyphrases
- extracellular matrix
- oxidative stress
- disease activity
- inflammatory response
- rheumatoid arthritis
- systemic lupus erythematosus
- induced apoptosis
- single molecule
- rheumatoid arthritis patients
- ankylosing spondylitis
- skeletal muscle
- juvenile idiopathic arthritis
- immune response
- binding protein
- cell cycle arrest
- cancer therapy
- drug delivery
- circulating tumor
- lps induced
- signaling pathway