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β2-glycoprotein I and Anti-β2-glycoprotein I Antibodies

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Conclusions

Because β2-GPI was found to be a major antigen for aPL, many studies have been focused on the physiological role of β2-GPI, on mechanism of thrombosis induced by anti-β2-GPI antibody, and on clinical significance of this autoantibody. Physiological roles of β2-GPI have been reported, although “true” property in human has yet to be determined. Several epitopes for anti-β2-GPI antibodies are known, however, all of the anti-β2-GPI antibodies may not be pathogenic and anti-β2-GPI antibodies are heterogeneous. What we learn from these clinical reports would be as follows. First, the standardization of the assay system for aPL is urgent. Second, measurement of aPL using multiple methods is favored in order to establish better assay for diagnosis and/or for prediction of disease activity. Last, more prospective, multi-center studies will be needed after standardization of the assay systems.

Recently, pathogenic roles of anti-β2-GPI antibodies have been reported in the fields of coagulation and fibrinolysis, atherosclerosis, or signal transduction and cell activation. These findings may contribute to better and specific therapies for patients with APS.

Keywords

  • Systemic Lupus Erythematosus
  • Lupus Anticoagulant
  • Anticardiolipin Antibody
  • Tropical Spastic Paraparesis
  • Negative Feedback Pathway

These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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© 2006 Springer-Verlag London Limited

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Yasuda, S., Atsumi, T., Koike, T. (2006). β2-glycoprotein I and Anti-β2-glycoprotein I Antibodies. In: Khamashta, M.A. (eds) Hughes Syndrome. Springer, London. https://doi.org/10.1007/1-84628-009-5_25

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  • DOI: https://doi.org/10.1007/1-84628-009-5_25

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