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Altered β2 -glycoprotein I expression on microparticles in the presence of antiphospholipid antibodies
F Mobarrez1, I Gunnarsson1, E Svenungsson1
1Unit of Rheumatology, Department of Medicine, Solna, Karolinska Institutet, Karolinska University Hospital, Stockholm, Sweden.
Abstract:
Essentials β2 glycoprotein-I (β2 GPI) is a scavenger molecule that binds to microparticles (MPs). β2 GPI expression on MPs was measured in systemic lupus erythematosus (SLE) patients and controls. β2 GPI positive MPs is depressed among SLE patients positive for antiphospholipid antibodies. Complex formation between β2 GPI on MPs and patients own anti-β2 GPI may disturb MP clearance. Click to hear an ISTH Academy presentation on antiphospholipid antibody syndrome by Drs de Laat and Bertolaccini SUMMARY: Background Antiphospholipid antibodies (aPLs) together with thrombosis and/or pregnancy morbidities characterize the antiphospholipid syndrome. β2 -Glycoprotein I (β2 GPI), the most important antigen for aPLs, is a scavenger molecule that specifically binds to phosphatidylserine (PS) expressed on microparticles (MPs). Objectives To evaluate β2 GPI-expressing MPs in patients with systemic lupus erythematosus (SLE) stratified for aPL status, and in healthy controls. Patients/Methods We investigated 18 aPL/anti-β2 GPI-positive and 22 aPL-negative patients from a large SLE cohort and 19 healthy controls. β2 GPI-positive MPs and IgG-positive MPs were detected by flow cytometry. We measured plasma levels of β2 GPI, and performed in vitro experiments to investigate the binding properties of β2 GPI on MPs. Results SLE patients had more MPs and IgG-positive MPs than controls. We observed fewer β2 GPI-positive MPs in aPL/anti-β2 GPI-positive patients than in aPL/anti-β2 GPI-negative patients and controls (approximately two-fold). β2 GPI levels in plasma did not differ with aPL/anti-β2 GPI status in patients; however, controls had slightly higher levels of β2 GPI than aPL/anti-β2 GPI-positive patients. In vitro experiments revealed that β2 GPI preferentially binds to PS-positive MPs. Conclusions Despite abundant total MPs and MPs in immune complexes, β2 GPI-positive MPs were depleted in SLE patients, and the levels were especially low in aPL/anti-β2 GPI-positive patients. We suggest that anti-β2 GPI antibodies bind to β2 GPI-PS complexes expressed on MPs. Consequent loss of β2 GPI-PS expression on MPs may impair scavenging and contribute to the accumulation of circulating PS-negative MPs, a possible source of autoantigens. Autoantibodies delaying MP clearance may thus constitute an important mechanism underlying autoimmunity.
Insights
Systemic lupus erythematosus patients with antiphospholipid antibodies have fewer beta2 glycoprotein-I positive microparticles. This reduction may impair microparticle clearance, contributing to autoimmune disease development.
Area of Science:
- Immunology
- Rheumatology
- Hematology
Background:
- Antiphospholipid antibodies (aPLs) and associated thrombosis/pregnancy issues define antiphospholipid syndrome.
- Beta2-glycoprotein I (β2GPI) is a key antigen for aPLs, acting as a scavenger molecule binding phosphatidylserine (PS) on microparticles (MPs).
Purpose of the Study:
- To evaluate β2GPI-expressing MPs in systemic lupus erythematosus (SLE) patients, stratified by aPL status, and in healthy controls.
- To investigate the role of β2GPI-PS complexes on MPs in the context of aPLs and SLE.
Main Methods:
- Flow cytometry was used to detect β2GPI-positive and IgG-positive MPs in 18 aPL/anti-β2GPI-positive SLE patients, 22 aPL-negative SLE patients, and 19 healthy controls.
- Plasma β2GPI levels were measured, and in vitro experiments assessed β2GPI binding to MPs.
Main Results:
- SLE patients exhibited higher levels of total MPs and IgG-positive MPs compared to controls.
- A significant reduction (approximately two-fold) in β2GPI-positive MPs was observed in aPL/anti-β2GPI-positive SLE patients compared to aPL-negative patients and controls.
- In vitro studies confirmed preferential binding of β2GPI to PS-positive MPs.
Conclusions:
- β2GPI-positive MPs are depleted in SLE patients, particularly in those with aPLs/anti-β2GPI antibodies.
- Anti-β2GPI antibodies likely bind to β2GPI-PS complexes on MPs, leading to reduced β2GPI expression.
- This impaired scavenging of MPs may contribute to the accumulation of circulating MPs and the pathogenesis of autoimmunity in SLE.
