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Anti- β 2-glycoprotein I (GPI) autoantibodies, annexin V binding and the anti-phospholipid syndrome by J. G. Hanly; S. A. Smith is a Immunology and Microbiology article available to read on EtoBox.

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## SUMMARY We examined the role of autoantibodies to β2-GPI and prothrombin (PT) in the inhibition of annexin V binding to cardiolipin (CL) and the association with clinical manifestations of the anti-phospholipid syndrome (APS). Plasma samples from 59 patients with anti-phospholipid (aPL) antibodies were studied. Affinity purification of total IgG and IgG anti-ß2-GPI antibodies was performed using staphylococcal protein A and phospholipid liposomes. Annexin V binding to CL was significantly inhibited by 31/59 (53%) aPL+ plasma samples. There was a significant association between annexin V inhibition and elevated levels of IgG anti-cardiolipin (aCL) (r = −0.62; P < 0.001), IgG anti-ß2-GPI (r = −0.67; P < 0.001) and a weaker association with lupus anti-coagulant (r = −0.27; P = 0.05). There was no association with other isotypes of aCL and anti-ß2-GPI or with anti-PT of any isotype. In patients with clinical manifestations of the APS there were higher levels of IgG aCL (median (range) Z score): 10.0 (0–17.6) versus 5.0 (0–16.1); P = 0.03), IgG anti-ß2-GPI (4.5 (0–11.3) versus 0.9 (0–9.7); P = 0.02) and greater inhibition of annexin V binding to CL (−3.4 (−11.4–0.6) versus−1.1 (−10.8

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Author

J. G. Hanly; S. A. Smith

Publisher

Oxford University Press (OUP)

Published

2000

Language

EN

Field

Immunology and Microbiology (Life Sciences)