Activated Complement System's Impact in Antiphospholipid Syndrome Thrombosis: From Pathophysiology to Treatment

Area of Science:

• Immunology
• Hematology
• Pathophysiology

Background:

• Antiphospholipid syndrome (APS) is the leading cause of acquired thrombophilia.
• The prevailing theory suggests a "double-hit" model involving antiphospholipid antibodies (aPL) and a secondary trigger for thrombosis.
• Chronic immune activation by aPL disrupts the protective role of immunothrombosis.

Purpose of the Study:

• To review the role of complement system dysregulation in APS-associated thrombosis.
• To identify potential therapeutic targets within the complement system for APS treatment.

Main Methods:

• Review of current research on complement system involvement in APS pathophysiology.
• Analysis of how aPL interact with complement components.
• Evaluation of the complement system as a therapeutic target.

Main Results:

• The complement system plays a critical role in driving thrombosis in APS.
• aPL contribute to complement system overactivation through interactions with platelets, β2-glycoprotein I, and complement factor H.
• Dysregulation of the complement system is central to APS pathogenesis.

Conclusions:

• The complement system is a key mediator of thrombosis in antiphospholipid syndrome.
• Targeting the complement system presents a promising therapeutic strategy for APS.
• Further research into targeted therapeutics is essential for precision medicine in APS.