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Updated: Feb 11, 2026

Depletion of Specific Cell Populations by Complement Depletion
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Complement involvement in antiphospholipid syndrome.

Houcine Hamidi1, Luc Darnige2, Marie-Agnès Dragon Durey3

  • 1Laboratoire d'immunologie biologique, Hôpital Européen Georges Pompidou, Paris, France; UMRS 1138 INSERM Equipe Inflammation, Complement and Cancer, Paris, France.

Immunology Letters
|February 9, 2026
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Summary

Antiphospholipid syndrome (APS) involves complement system activation. Measuring complement fragments like C4d and C5a can guide personalized therapies for APS patients, improving treatment outcomes.

Keywords:
Anti-phospholipid antibodyComplementThrombosis

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Area of Science:

  • Immunology
  • Hematology
  • Pathophysiology

Background:

  • Antiphospholipid syndrome (APS) is an acquired thrombophilia with thrombotic and non-thrombotic manifestations.
  • The complement system plays a significant role in APS pathophysiology, interacting with the coagulation cascade.
  • Animal models and patient studies highlight complement's involvement in APS-related thrombosis and fetal morbidity.

Purpose of the Study:

  • To investigate the role of complement activation in Antiphospholipid syndrome (APS).
  • To explore the utility of complement activation fragments as biomarkers in APS.
  • To evaluate complement-targeting therapies for APS management.

Main Methods:

  • Analysis of complement activation fragments (C4d, C3a, C5a, sC5b9) in plasma and on blood cells.
  • Examination of complement deposition on affected tissues in APS patients.
  • Review of clinical data on complement-blocking therapies like eculizumab.

Main Results:

  • Complement activation is detectable in APS patients via plasma fragments and tissue deposition.
  • Specific fragments (C4d, C5a, sC5b9) indicate activation of different complement pathways.
  • Eculizumab (anti-C5 antibody) shows promise in severe APS cases, but requires standardization.

Conclusions:

  • Complement biomarkers are crucial for assessing APS activity and therapeutic efficacy.
  • Personalized treatment strategies for APS may involve targeting specific complement pathways.
  • Further standardized studies are needed to optimize complement-based therapies for APS.