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  • American Society of Hematology  (6)
  • Urbanus, Rolf T.  (6)
  • 1
    Online Resource
    Online Resource
    IgG antibodies that recognize epitope Gly40-Arg43 in domain I of β2–glycoprotein I cause LAC, and their presence correlates strongly with thrombosis
    American Society of Hematology ; 2005
    In:  Blood Vol. 105, No. 4 ( 2005-02-15), p. 1540-1545
    Details
    In: Blood, American Society of Hematology, Vol. 105, No. 4 ( 2005-02-15), p. 1540-1545
    Abstract: Anti–β2–glycoprotein I antibodies are known to have a heterogeneous reactivity against β2–glycoprotein I. We performed this study to characterize the epitope on β2–glycoprotein I to which pathologic anti–β2–glycoprotein I antibodies are directed. Plasma samples from 198 patients with various systemic autoimmune diseases were tested for the presence of lupus anticoagulant and anti–β2–glycoprotein I immunoglobulin G (IgG) antibodies. The reactivity of the anti–β2–glycoprotein I–positive samples was further tested by coating recombinant full-length β2–glycoprotein I and 8 deletion mutants of β2–glycoprotein I onto hydrophilic and hydrophobic enzyme-linked immunosorbent assay (ELISA) plates. Full-length β2–glycoprotein I with point mutations in domain I at positions 8, 40, and 43 were used in inhibition experiments. Fifty-two patients with anti–β2–glycoprotein I IgG antibodies could be divided into 2 patterns. Type A antibodies only recognize domain I when coated onto hydrophobic plates; they do not recognize domain I coated onto hydrophilic plates. Type B antibodies have heterogeneous reactivity for all domains. Type A antibodies recognize the epitope around amino acids Gly40-Arg43 and cause lupus anticoagulant activity. In contrast to type B antibodies, those of type A strongly correlated with thrombosis. In conclusion, antibodies directed at domain I (epitope comprising Gly40 and Arg43) have lupus anticoagulant activity and strongly associate with thrombosis.
    Type of Medium: Online Resource
    ISSN: 0006-4971 , 1528-0020
    URL: Article
    DOI: 10.1182/blood-2004-09-3387
    RVK:
    XA 33000
    RVK:
    XA 10000
    Language: English
    Publisher: American Society of Hematology
    Publication Date: 2005
    detail.hit.zdb_id: 1468538-3
    detail.hit.zdb_id: 80069-7
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  • 2
    Online Resource
    Online Resource
    Decreased beta2-Glycoprotein I Plasma Levels as a Risk Factor for Myocardial Infarction in Men.
    American Society of Hematology ; 2008
    In:  Blood Vol. 112, No. 11 ( 2008-11-16), p. 1813-1813
    Details
    In: Blood, American Society of Hematology, Vol. 112, No. 11 ( 2008-11-16), p. 1813-1813
    Abstract: Background: Several factors influence the occurrence of acute myocardial infarction. One of these factors is thought to be Von Willebrand Factor which serves as adhesive surface for platelets to adhere to the vessel wall. We have recently found that beta2- glycoprotein I is able to inhibit platelet binding to von Willebrand Factor by binding to the A1 domain of Von Willebrand Factor 1. This could indicate that beta2-glycoprotein I possesses antithrombotic properties with respect to arterial thrombosis. In the present study we investigated whether differences in beta2-glycoprotein I plasma levels influence the risk of myocardial infarction. Methods and Results: We have measured beta2-glycoprotein I and Von Willebrand Factor antigen levels in 539 men with a first myocardial infarction and in 611 control subjects who participated in the case-control Study of Myocardial Infarction Leiden (SMILE). Although we did not find a profound effect of beta2-glycoprotein I plasma levels on myocardial infarction in the overall population (odds ratio 0.93, 95% confidence interval 0.65–1.33), there appeared to be a dose-dependent protective effect of increasing beta2-glycoprotein I plasma levels on myocardial infarction in men of 60 years and older. In this age group we found an odds Ratio of 0.44 (95% confidence interval 0.25–0.77) for high beta2-glycoprotein I levels compared to low levels. Furthermore, high plasma levels of beta2-glycoprotein I remained protective for myocardial infarction despite high levels of Von Willebrand Factor. In addition, we studied a possible association between age and Von Willebrand Factor and beta2-glycoprotein I plasma levels. It appeared that both Von Willebrand Factor and beta2-glycoprotein I plasma levels increased with age, but a larger increase in Von Willebrand Factor plasma levels was observed than in beta2-glycoprotein I plasma levels (13.7 % every 10 years versus 5.7% every 10 years). Conclusions: In this study high circulating levels of beta2-glycoprotein I appeared to be associated with a lower risk of myocardial infarction in men over 60 years. In addition we observed a larger increase in Von Willebrand Factor levels with age than beta2- glycoprotein I levels. As beta2-glycoprotein I possesses antithrombotic properties by inhibiting the activity of Von Willebrand Factor in-vitro, this might indicate that during aging the haemostatic balance slowly shifts to a more prothrombotic state 1. Future in-vivo experiments are needed to investigate the exact contribution of beta2-glycoprotein I on the pathophysiology of myocardial infarction and arterial thrombosis in general.
    Type of Medium: Online Resource
    ISSN: 0006-4971 , 1528-0020
    URL: Article
    DOI: 10.1182/blood.V112.11.1813.1813
    RVK:
    XA 33000
    RVK:
    XA 10000
    Language: English
    Publisher: American Society of Hematology
    Publication Date: 2008
    detail.hit.zdb_id: 1468538-3
    detail.hit.zdb_id: 80069-7
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  • 3
    Online Resource
    Online Resource
    β2-glycoprotein I–dependent lupus anticoagulant highly correlates with thrombosis in the antiphospholipid syndrome
    American Society of Hematology ; 2004
    In:  Blood Vol. 104, No. 12 ( 2004-12-01), p. 3598-3602
    Details
    In: Blood, American Society of Hematology, Vol. 104, No. 12 ( 2004-12-01), p. 3598-3602
    Abstract: The antiphospholipid syndrome is characterized by the presence of antiphospholipid antibodies in plasma of patients with thromboembolic complications. A major problem in defining the syndrome is that serologic assays to detect antiphospholipid antibodies have a low specificity. We recently published a method that specifically detects lupus anticoagulant (LAC) caused by anti–β2-glycoprotein I antibodies. Here, we studied the clinical relevance of detecting β2-glycoprotein I–dependent LAC. Plasma samples were collected from 198 patients with autoimmune diseases. In those samples with a positive partial thromboplastin time–lupus anticoagulant (PTT-LA), a modified activated partial thromboplastin time (aPTT)–based LAC test was performed with cardiolipin as confirming agent. Twenty-five of 58 patients with an aPTT-based LAC were dependent on the presence of anti–β2-glycoprotein I antibodies. Presence of β2-glycoprotein I–dependent LAC was almost completely associated with a history of thromboembolic complications (odds ratio, 42.3; 95% confidence interval, 194.3-9.9). An increased frequency of thrombosis was not found in 33 patients with LAC independent of anti–β2-glycoprotein I antibodies (odds ratio, 1.6; 95% confidence interval, 3.9-0.8). The use of an LAC assay with cardiolipin as confirming agent strongly improves the detection of patients at risk of thrombosis. Our findings suggest that anti–β2-glycoprotein I antibodies with LAC activity are antibodies that are responsible for the thromboembolic complications in the antiphospholipid syndrome.
    Type of Medium: Online Resource
    ISSN: 0006-4971 , 1528-0020
    URL: Article
    DOI: 10.1182/blood-2004-03-1107
    RVK:
    XA 33000
    RVK:
    XA 10000
    Language: English
    Publisher: American Society of Hematology
    Publication Date: 2004
    detail.hit.zdb_id: 1468538-3
    detail.hit.zdb_id: 80069-7
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  • 4
    Online Resource
    Online Resource
    Association between beta2-glycoprotein I plasma levels and the risk of myocardial infarction in older men
    American Society of Hematology ; 2009
    In:  Blood Vol. 114, No. 17 ( 2009-10-22), p. 3656-3661
    Details
    In: Blood, American Society of Hematology, Vol. 114, No. 17 ( 2009-10-22), p. 3656-3661
    Abstract: von Willebrand factor (VWF) serves as adhesive surface for platelets to adhere to the vessel wall. We have recently found that beta2-glycoprotein I is able to inhibit platelet binding to VWF, indicating a role in the pathophysiology of arterial thrombosis. In the present study, we investigated whether differences in beta2-glycoprotein I plasma levels influence the risk of myocardial infarction. We have measured beta2-glycoprotein I and VWF antigen levels in 539 men with a first myocardial infarction and in 611 control subjects. Although we did not find a profound effect of beta2-glycoprotein I plasma levels on myocardial infarction in the overall population, we found a dose-dependent protective effect of increasing beta2-glycoprotein I plasma levels on myocardial infarction in men 60 years and older. In this age group, we found an odds ratio of 0.41 (95% confidence interval, 0.22-0.74) for high beta2-glycoprotein I levels compared with low levels. High plasma levels of beta2-glycoprotein I remained protective for myocardial infarction despite high levels of VWF. To conclude, high circulating levels of beta2-glycoprotein I appeared to be associated with a reduced risk of myocardial infarction in elderly men. In vivo experiments are needed to investigate the exact contribution of beta2-glycoprotein I on the pathophysiology of myocardial infarction.
    Type of Medium: Online Resource
    ISSN: 0006-4971 , 1528-0020
    URL: Article
    DOI: 10.1182/blood-2009-03-212910
    RVK:
    XA 33000
    RVK:
    XA 10000
    Language: English
    Publisher: American Society of Hematology
    Publication Date: 2009
    detail.hit.zdb_id: 1468538-3
    detail.hit.zdb_id: 80069-7
    Location Call Number Limitation Availability
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    Online Resource
  • 5
    Online Resource
    Online Resource
    Apolipoprotein E receptor 2 is involved in the thrombotic complications in a murine model of the antiphospholipid syndrome
    American Society of Hematology ; 2011
    In:  Blood Vol. 117, No. 4 ( 2011-01-27), p. 1408-1414
    Details
    In: Blood, American Society of Hematology, Vol. 117, No. 4 ( 2011-01-27), p. 1408-1414
    Abstract: Antiphospholipid (aPL)/anti-β2 glycoprotein I (anti-β2GPI) antibodies stimulates tissue factor (TF) expression within vasculature and in blood cells, thereby leading to increased thrombosis. Several cellular receptors have been proposed to mediate these effects, but no convincing evidence for the involvement of a specific one has been provided. We investigated the role of Apolipoprotein E receptor 2 (ApoER2′) on the pathogenic effects of a patient-derived polyclonal aPL IgG preparation (IgG-APS), a murine anti-β2GPI monoclonal antibody (E7) and of a constructed dimeric β2GPI I (dimer), which in vitro mimics β2GPI-antibody immune complexes, using an animal model of thrombosis, and ApoER2-deficient (−/−) mice. In wild type mice, IgG-APS, E7 and the dimer increased thrombus formation, carotid artery TF activity as well as peritoneal macrophage TF activity/expression. Those pathogenic effects were significantly reduced in ApoER2 (−/−) mice. In addition, those effects induced by the IgG-APS, by E7 and by the dimer were inhibited by treatment of wild-type mice with soluble binding domain 1 of ApoER2 (sBD1). Altogether these data show that ApoER2 is involved in pathogenesis of antiphospholipids antibodies.
    Type of Medium: Online Resource
    ISSN: 0006-4971 , 1528-0020
    URL: Article
    DOI: 10.1182/blood-2010-07-299099
    RVK:
    XA 33000
    RVK:
    XA 10000
    Language: English
    Publisher: American Society of Hematology
    Publication Date: 2011
    detail.hit.zdb_id: 1468538-3
    detail.hit.zdb_id: 80069-7
    Location Call Number Limitation Availability
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  • 6
    Online Resource
    Online Resource
    β2-Glycoprotein I can exist in 2 conformations: implications for our understanding of the antiphospholipid syndrome
    American Society of Hematology ; 2010
    In:  Blood Vol. 116, No. 8 ( 2010-08-26), p. 1336-1343
    Details
    In: Blood, American Society of Hematology, Vol. 116, No. 8 ( 2010-08-26), p. 1336-1343
    Abstract: The antiphospholipid syndrome is defined by the presence of antiphospholipid antibodies in blood of patients with thrombosis or fetal loss. There is ample evidence that β2-glycoprotein I (β2GPI) is the major antigen for antiphospholipid antibodies. The autoantibodies recognize β2GPI when bound to anionic surfaces and not in solution. We showed that β2GPI can exist in at least 2 different conformations: a circular plasma conformation and an “activated” open conformation. We also showed that the closed, circular conformation is maintained by interaction between the first and fifth domain of β2GPI. By changing pH and salt concentration, we were able to convert the conformation of β2GPI from the closed to the open conformation and back. In the activated open conformation, a cryptic epitope in the first domain becomes exposed that enables patient antibodies to bind and form an antibody-β2GPI complex. We also demonstrate that the open conformation of β2GPI prolonged the activated partial thromboplastin time when added to normal plasma, whereas the activated partial thromboplastin time is further prolonged by addition of anti-β2GPI antibodies. The conformational change of β2GPI, and the influence of the autoantibodies may have important consequences for our understanding of the antiphospholipid syndrome.
    Type of Medium: Online Resource
    ISSN: 0006-4971 , 1528-0020
    URL: Article
    DOI: 10.1182/blood-2009-12-260976
    RVK:
    XA 33000
    RVK:
    XA 10000
    Language: English
    Publisher: American Society of Hematology
    Publication Date: 2010
    detail.hit.zdb_id: 1468538-3
    detail.hit.zdb_id: 80069-7
    Location Call Number Limitation Availability
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