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NETs in APS: Current Knowledge and Future Perspectives.

Ajay Tambralli1,2, Kelsey Gockman2, Jason S Knight3

  • 1Division of Pediatric Rheumatology, Department of Pediatrics, University of Michigan, Ann Arbor, MI, USA.

Current Rheumatology Reports
|August 27, 2020
PubMed
Summary
This summary is machine-generated.

Neutrophils and neutrophil extracellular traps (NETs) play a key role in antiphospholipid syndrome (APS) inflammation and thrombosis. Targeting NETs offers promising new therapeutic strategies for APS patients.

Keywords:
Antiphospholipid syndromeInterferonsNeutrophil extracellular trapsNeutrophilsReactive oxygen species

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Area of Science:

  • Immunology
  • Hematology
  • Rheumatology

Background:

  • Antiphospholipid syndrome (APS) is a thrombo-inflammatory condition primarily managed with anticoagulation.
  • Understanding the inflammatory mechanisms in APS is crucial for developing improved and personalized treatments.

Purpose of the Study:

  • To review recent literature on the involvement of neutrophils and neutrophil extracellular traps (NETs) in the pathophysiology of APS.

Main Methods:

  • Literature review focusing on the role of neutrophils and NETs in APS.
  • Analysis of gene expression patterns in APS neutrophils.
  • Investigation of NET release thresholds and reactive oxygen species in APS.

Main Results:

  • APS neutrophils exhibit increased expression of genes related to type I interferons, endothelial adhesion, and pregnancy regulation.
  • Neutrophils in APS have a lower threshold for NET release, potentially exacerbating thrombotic events, particularly large-vein thrombosis.
  • Neutrophil-derived reactive oxygen species contribute to APS pathogenesis.

Conclusions:

  • Neutrophils and NETs are significant contributors to APS pathophysiology.
  • Further mechanistic understanding of neutrophils and NETs can identify novel therapeutic targets.
  • Strategies targeting NET formation, dissolution, and neutrophil adhesion may improve APS management and reduce disease burden.