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Comprehensive Analysis of Procoagulant Platelets Exhibiting Features of Necrosis, Apoptosis and Platelet Activation

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Complement and thrombosis in the antiphospholipid syndrome.

Kenji Oku¹, Hiroyuki Nakamura¹, Michihiro Kono¹

¹Department of Rheumatology, Endocrinology and Nephrology, Hokkaido University Graduate School of Medicine, Sapporo, Japan.

Autoimmunity Reviews

|August 4, 2016

Summary

Autoantibodies against C1q are linked to complement activation in antiphospholipid syndrome (APS). Higher levels in refractory APS patients suggest a role in disease severity and thrombotic events.

Keywords:

Anti-C1q antibody Antiphospholipid antibody Antiphospholipid syndrome Complement pathway

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Area of Science:

Immunology
Rheumatology
Pathophysiology

Background:

Complement activation is implicated in antiphospholipid syndrome (APS) pathophysiology.
Previous research indicated complement activation in APS sera contributes to procoagulant cell activation.
Autoantibodies against C1q correlate with complement activation in systemic lupus erythematosus.

Purpose of the Study:

To investigate the prevalence and significance of anti-C1q antibodies in primary and refractory APS patients.
To explore the association between anti-C1q antibodies, complement activation, and thrombotic events in APS.

Main Methods:

Detection of anti-C1q antibodies in primary APS, refractory APS, and control patient sera.
Comparison of anti-C1q antibody titers between APS patient subgroups (refractory vs. non-flare).

Main Results:

Anti-C1q antibodies were detected more frequently in primary APS patients compared to controls.
Refractory APS patients with recurrent thrombotic events showed higher anti-C1q antibody titers.
Significantly higher anti-C1q antibody titers were observed in refractory APS patients compared to those without flare.

Conclusions:

Anti-C1q antibodies are more prevalent in APS patients, particularly those with refractory disease and thrombotic events.
Elevated anti-C1q antibodies may indicate accelerated complement activation in APS, potentially exacerbated by 'second-hit' stressors.
The binding of C1q to anionic phospholipids, targeted by anti-C1q antibodies, could drive complement activation surges in APS.