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Targeting thromboinflammation in antiphospholipid syndrome.

Dorien M Salet1, Siroon Bekkering2, Saskia Middeldorp2

  • 1Department of Vascular Medicine, Amsterdam UMC, Amsterdam, The Netherlands.

Journal of Thrombosis and Haemostasis : JTH
|January 25, 2023
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Summary

Antiphospholipid syndrome (APS) involves antiphospholipid antibodies (aPL) causing blood clots and pregnancy issues. Understanding its thromboinflammation mechanisms reveals new therapeutic targets for APS and similar diseases.

Keywords:
antiphospholipid syndromeimmunomodulationmonocytesneutrophilsthromboinflammation

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Area of Science:

  • Immunology
  • Cardiovascular Medicine
  • Rheumatology

Background:

  • Antiphospholipid syndrome (APS) is an autoimmune disorder characterized by antiphospholipid antibodies (aPL).
  • APS links inflammation and thrombosis, contributing to cardiovascular disease pathophysiology.
  • It serves as a model for studying thromboinflammation and innate immunity's role in thrombosis.

Purpose of the Study:

  • To review the mechanisms of thromboinflammation in APS.
  • To identify cellular pathways and interactions involved in APS pathogenesis.
  • To highlight potential therapeutic targets for APS and other thromboinflammatory diseases.

Main Methods:

  • Review of scientific literature on APS, thromboinflammation, and innate immune cell activation.
  • Analysis of cellular signaling pathways including NF-κB, mTOR, and inflammasomes.
  • Examination of neutrophil extracellular trap (NET) formation and platelet activation in APS.

Main Results:

  • aPL activate monocytes, promoting a pro-inflammatory and pro-coagulant state via cytokines and tissue factor.
  • Neutrophils contribute to thrombosis through NETosis and enhanced interactions with endothelial cells.
  • Platelet activation by aPL increases platelet-leukocyte interactions, contributing to a pro-coagulant phenotype.

Conclusions:

  • Targeting pathways like NF-κB, mTOR, and inflammasomes offers therapeutic potential in APS.
  • Interventions against NETosis and platelet activation present viable treatment strategies.
  • Understanding APS thromboinflammation mechanisms can inform treatments for broader cardiovascular and autoimmune conditions.