Platelet activation and anti-phospholipid antibodies collaborate in the activation of the complement system on platelets in systemic lupus erythematosus

• Published in: PloS one 2014-06, Vol.9 (6), p.e99386-e99386
• Main Authors: Lood, Christian, Tydén, Helena, Gullstrand, Birgitta, Sturfelt, Gunnar, Jönsen, Andreas, Truedsson, Lennart, Bengtsson, Anders A
• Format: Article
• Language: English
• Subjects: Adolescent; Adult; Aged; Aged, 80 and over; Antibodies; Antibodies, Antiphospholipid - immunology; Antiphospholipid antibodies; Arthritis; Autoimmune diseases; Basic Medicine; Biology and Life Sciences; Blood platelets; Blood Platelets - immunology; Cardiolipins - immunology; Cardiovascular disease; Cardiovascular diseases; Chronic conditions; Classical pathway; Clinical Medicine; Complement; Complement activation; Complement Activation - immunology; Complement C4b - immunology; Complement component C1q; Deposition; Female; Health risks; Heart attacks; Hospitals; Humans; Immunoglobulins; Immunologi inom det medicinska området; Immunology; Immunology in the medical area; Inflammatory diseases; Kinases; Klinisk medicin; Laboratories; Lupus; Lupus Erythematosus, Systemic - blood; Lupus Erythematosus, Systemic - immunology; Male; Medical and Health Sciences; Medicin och hälsovetenskap; Medicine and Health Sciences; Medicinska och farmaceutiska grundvetenskaper; Microbiology in the medical area; Middle Aged; Mikrobiologi inom det medicinska området; Mortality; Patients; Peptide Fragments - immunology; Phospholipids; Platelet Activation - immunology; Platelets; Reumatologi och inflammation; Rheumatic diseases; Rheumatoid arthritis; Rheumatoid factor; Rheumatology; Rheumatology and Autoimmunity; Risk analysis; Risk Factors; Shipping industry; Stroke; Studies; Systemic lupus erythematosus; Systemic sclerosis; Thromboembolism; Thrombosis; Thrombosis - blood; Thrombosis - immunology; Young Adult
• ISSN: 1932-6203; 1932-6203
• DOI: 10.1371/journal.pone.0099386

Anti-phospholipid (aPL) antibodies are important contributors to development of thrombosis in patients with the autoimmune rheumatic disease systemic lupus erythematosus (SLE). The underlying mechanism of aPL antibody-mediated thrombosis is not fully understood but existing data suggest that platelets and the complement system are key components. Complement activation on platelets is seen in SLE patients, especially in patients with aPL antibodies, and has been related to venous thrombosis and stroke. The aim of this study was to investigate if aPL antibodies could support classical pathway activation on platelets in vitro as well as in SLE patients. Furthermore, we investigated if complement deposition on platelets was associated with vascular events, either arterial or venous, when the data had been adjusted for traditional cardiovascular risk factors. Finally, we analyzed if platelet complement deposition, both C1q and C4d, was specific for SLE. We found that aPL antibodies supported C4d deposition on platelets in vitro as well as in SLE patients (p = 0.001 and p