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Journal of Immunology Research
Volume 2015 (2015), Article ID 638129, 12 pages
Research Article

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

1Department for Internal Medicine 3, University Hospital Erlangen, Friedrich-Alexander-Universität Erlangen-Nürnberg (FAU), Ulmenweg 18, 91054 Erlangen, Germany
2Institute of Cell Biology, National Academy of Sciences of Ukraine, Drahomanov Street 14/16, Lviv 79005, Ukraine
3Department of Otorhinolaryngology, Head and Neck Surgery, Section for Experimental Oncology and Nanomedicine (SEON), University Hospital, Waldstraße 1/Glückstraße 10, 91054 Erlangen, Germany
4Rheumatology and Clinical Immunology, Department of Clinical and Experimental Sciences, Spedali Civili and University of Brescia, Piazzale Spedali Civili 1, 25123 Brescia, Italy
5Paediatric Immunology and Rheumatology, Children’s Hospital Brescia, Department of Clinical and Experimental Sciences, Spedali Civili and University of Brescia, Piazzale Spedali Civili 1, 25123 Brescia, Italy
6Department of Biology, Institute of Genetics, Friedrich-Alexander-Universität Erlangen-Nürnberg (FAU), Erwin-Rommel Str. 3, 91058 Erlangen, Germany

Received 11 February 2015; Accepted 12 May 2015

Academic Editor: Kurt Blaser

Copyright © 2015 Christoph Fickentscher et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


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.