Mechanism of Thrombosis in Antiphospholipid Syndrome: Binding to Platelets

Reverter, Joan Carles; Tàssies, Dolors

doi:10.1007/1-84628-009-5_32

Cited by 4 publications

(3 citation statements)

References 81 publications

(105 reference statements)

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“…The activation is accompanied by platelet aggregation and the release of mediators such as the prothrombotic Thromboxane A2 [ 50 ]. Consecutively, this cascade can result in thrombus formation [ 51 , 52 ]. Sialylated anti- β 2GP1-IgG is unable to bind to and to activate platelets via Fc γ RIIA.…”

Section: Discussionmentioning

confidence: 99%

The Pathogenicity of Anti-β2GP1-IgG Autoantibodies Depends on Fc Glycosylation

Fickentscher

Magorivska

Janko

et al. 2015

Journal of Immunology Research

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To analyze the glycosylation of anti-β2GP1, we investigated purified IgG from healthy children, patients with APS, and asymptomatic adult carriers of antiphospholipid antibodies. We observed that in the sera of healthy children and of patients with APS, IgG3 and IgG2 were predominant, respectively. The potentially protective anti-β2GP1-IgM was lower in the sera of healthy children. Although anti-β2GP1-associated C1q did not differ between children and patients with antiphospholipid syndrome, the associated C3c was significantly higher in the sera of healthy children. This indicates a more efficient clearance of anti-β2GP1 immune complexes in the healthy children. This clearance is not accompanied by inflammation or coagulatory events. It is likely that the most important pathogenic factor of the anti-β2GP1-IgG is related to the different glycosylation observed in healthy and diseased individuals. We detected a significantly higher sialylation of anti-β2GP1-IgG isolated from the sera of healthy children and asymptomatic adults when compared with that of patients with clinically apparent antiphospholipid syndrome. Low sialylated IgG reportedly ameliorates inflammation and inflammation promotes hyposialylation. Thus, both reactions create a vicious circle that precipitates the pathology of the antiphospholipid syndrome including thrombus-formation. We conclude that the increased sialylation of anti-β2GP1-IgG of sera of healthy individuals limits their pathogenicity.

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Section: Discussionmentioning

confidence: 99%

The Pathogenicity of Anti-β2GP1-IgG Autoantibodies Depends on Fc Glycosylation

Fickentscher

Magorivska

Janko

et al. 2015

Journal of Immunology Research

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“…However, not all groups have confirmed the ability of aPL or anti β 2 GPI antibodies to activate platelets [82]. The picture is complicated by the presence of specific antiplatelet antibodies in the serum of patients with APS and associated connective tissue diseases.…”

Section: Haemostasismentioning

confidence: 99%

Antiphospholipid syndrome: multiple mechanisms

Mackworth‐Young

2004

Clinical and Experimental Immunology

102

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“…Bei der Thrombusformation wird die Interaktion der aPL sowohl mit den Thrombozyten als auch den Endothelzellen als bedeutsam eingestuft [20,24]. Vaarala et al sehen eine Erklä-rung in der Interferenz der aPL mit Bestandteilen der Blutgerinnung [29], woraus eine Verschiebung der Hämostase in Richtung Hyperkoagulabilität resultiert.…”

Section: Diskussionunclassified

Oxidativ modifizierte Lipoproteine und deren Antik�rper bei Patienten mit Antiphospholipidsyndrom und Systemischem Lupus erythematodes

et al. 2004

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The antiphospholipid syndrome (APS) with its typical clinical manifestations of recurrent thrombosis and fetal loss is biochemically defined by the presence of circulating antiphospholipid antibodies (aPL). The disease pattern has raised special interest as a possible link between autoimmunity and atherosclerosis. aPL, oxidized low density lipoproteins (oxLDL), and antibodies to oxLDL (Anti-oxLDL) are suggested to play an important role in atherogenesis. In the present study we compared the serum levels of oxLDL and Anti-oxLDL in APS patients (20 subjects with primary APS; 14 subjects with secondary APS) and nonAPS subjects (24 phenotypically healthy controls samples and 12 patients with systemic lupus erythematosus [SLE]) and investigated associations of the above mentioned parameters with the intima-media thickness (IMT), a clinical surrogate parameter of atherosclerosis.SLE patients with and without APS showed significantly increased levels of Anti-oxLDL as compared to the controls group (p = 0.038 and p = 0.007, respectively). In contrast, oxLDL levels were not significantly different between the controls group and patients. The Anti-oxLDL levels correlated significantly with anticardiolipin (p = 0.002) and beta(2)-glycoprotein I antibodies (p < 0.048), both from IgG isotype. Only SLE patients without APS revealed a significantly elevated production of reactive oxygen species indicating an increased proatherogenic oxidative stress in the circulation (p < 0.002). In the patient groups, the circulating levels of oxLDL and Anti-oxLDL showed no association with atherosclerosis as estimated by IMT. In conclusion, our experimental data do not support the concept of oxidative stress-induced accelerated atherosclerosis in APS patients.

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Mechanism of Thrombosis in Antiphospholipid Syndrome: Binding to Platelets

Cited by 4 publications

References 81 publications

The Pathogenicity of Anti-β2GP1-IgG Autoantibodies Depends on Fc Glycosylation

The Pathogenicity of Anti-β2GP1-IgG Autoantibodies Depends on Fc Glycosylation

Antiphospholipid syndrome: multiple mechanisms

Oxidativ modifizierte Lipoproteine und deren Antik�rper bei Patienten mit Antiphospholipidsyndrom und Systemischem Lupus erythematodes

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