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The role of complement in the antiphospholipid syndrome-associated pathology

Ingrid Avalos1, George C Tsokos

  • 1Division of Rheumatology, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215, USA. iavalos@bidmc.harvard.edu

Clinical Reviews in Allergy & Immunology
|December 11, 2008
PubMed

Insights

Antiphospholipid syndrome (APS) involves blood clots and pregnancy loss, driven by antiphospholipid antibodies. Complement pathway activation is increasingly recognized as a key factor in APS development and severity.

Area of Science:

  • Immunology
  • Hematology
  • Reproductive Medicine

Background:

  • Antiphospholipid syndrome (APS) is an autoimmune disorder.
  • Characterized by thrombosis, pregnancy morbidity, and antiphospholipid antibodies.
  • Pathogenic mechanisms remain incompletely understood.

Purpose of the Study:

  • To investigate the role of complement activation in APS pathogenesis.
  • To explore the contribution of complement to pregnancy morbidity and thrombosis in APS.

Main Methods:

  • Utilized complement-deficient murine models.
  • Studied features of pregnancy morbidity and thrombosis in these models.

Main Results:

  • Complement activation plays a significant role in APS pathogenesis.
  • Complement deficiency impacts thrombosis and pregnancy outcomes in APS models.

Conclusions:

  • Complement activation is a key contributor to APS.
  • Complement-deficient models provide insights into APS mechanisms.
  • Findings support developing new therapeutic strategies targeting the complement pathway for APS management.

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