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Related Experiment Videos

Antiphospholipid antibody-dependent C5b-9 formation

M W Stewart1, W S Etches, P A Gordon

  • 1Department of Laboratory Medicine and Pathology, University of Alberta Hospitals, Edmonton, Canada.

British Journal of Haematology
|March 1, 1997
PubMed
Summary
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Antiphospholipid antibodies (APA) trigger complement system activation, leading to platelet damage. This study demonstrates that the terminal membrane attack complex (MAC) of complement is involved in APA-mediated platelet destruction, suggesting a key role for complement in this process.

Area of Science:

  • Immunology
  • Hematology
  • Complement System

Background:

  • Antiphospholipid antibodies (APA) are associated with thrombosis and pregnancy complications.
  • The role of the complement system in APA-mediated pathology is not fully understood.
  • Platelet activation and destruction are observed in patients with APA.

Purpose of the Study:

  • To investigate the relationship between antiphospholipid antibodies (APA) and the production of the terminal membrane attack complex (MAC) of complement (C5b-9).
  • To determine if complement activation is involved in APA-induced platelet damage.

Main Methods:

  • Studied serum samples from patients with high positive APA.
  • Utilized heat-inactivation, serum supplementation, and adsorption techniques to assess complement involvement.

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  • Employed monoclonal antibodies against C5b-9 (aE11) to block MAC formation.
  • Used flow cytometry to detect C5b-9 formation and binding to phospholipid-coated beads.
  • Analyzed 200 serum samples for APA and C5b-9 production.

    • Main Results:

    • APA-positive sera induced platelet activation and destruction, inhibited by heat-inactivation and restored by normal serum.
    • Adsorption of APA with phospholipid-coated beads and addition of anti-C5b-9 mAb inhibited platelet destruction.
    • Purified APA induced C5b-9 formation in a dose-dependent manner.
    • All sera negative for APA were also negative for C5b-9 production.
    • High levels of IgG binding to phospholipids (GPL) correlated with C5b-9 production.

    Conclusions:

    • Complement activation, specifically the formation of C5b-9, plays a significant role in APA-dependent platelet activation and destruction.
    • The terminal complement pathway is implicated in the pathogenesis of antiphospholipid syndrome.
    • These findings suggest complement inhibition as a potential therapeutic strategy for APA-related conditions.