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By A. Bulikova

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1993) Identification of a region of beta 2-glycoprotein I critical for lipid binding and anti-cardiolipin antibody cofactor activity. Proc Natl Acad Sci U S A. 90(6), 2141-2145. Ikematsu W, Luan FL, La Rosa L, Beltrami B, Nicoletti F, Buyon JP, Meroni PL, Balestrieri G & Casali P. (1998) Human anticardiolipin monoclonal autoantibodies cause placental necrosis and fetal loss in BALB/c mice. Arthritis Rheum. 41(6), 10261039. Iverson GM, Victoria EJ & Marquis DM. (1998) Anti-beta2 glycoprotein I (beta2GPI) autoantibodies recognize an epitope on the first domain of beta2GPI.

Despite much research effort over the last 25 years, we do not know how aPL increases the risk of thrombosis and recurrent fetal loss in patients with APS. Many theories have been proposed to explain the increased thrombotic tendency in patients with aPL, but unfortunately none of them has been proven by convincing evidence. 2. Antiphospholipid antibody syndrome: Phenotype assessment In the decades following the recognition of APS as a distinct entity, there came increasing calls for a consensus on the criteria required for accurate diagnosis of these patients.

2GPI’s alternative name, apolipoprotein H, suggests a function in lipid metabolism, but this was based on a single publication that dates from 1979 in which it was shown that β2GPI was distributed over different human lipoproteins (Polz & Kostner, 1979). , 1983), and the official designation for the β2GPI gene has become APOH. , 1990). , 1999). In this chapter we will focus on this novel conformation of β2GPI and discuss the consequences of the transition between the two conformations for β2GPI on past but also on present findings.

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