Antiphospholipid antibodies affect trophoblast gonadotropin secretion and invasiveness by binding directly and through adhered β2-glycoprotein I
Article first published online: 2 APR 2001
Copyright © 2000 by the American College of Rheumatology
Arthritis & Rheumatism
Volume 43, Issue 1, pages 140–150, January 2000
How to Cite
Di Simone, N., Meroni, P. L., Del Papa, N., Raschi, E., Caliandro, D., De Carolis, S., Khamashta, M. A., Atsumi, T., Hughes, G. R. V., Balestrieri, G., Tincani, A., Casali, P. and Caruso, A. (2000), Antiphospholipid antibodies affect trophoblast gonadotropin secretion and invasiveness by binding directly and through adhered β2-glycoprotein I. Arthritis & Rheumatism, 43: 140–150. doi: 10.1002/1529-0131(200001)43:1<140::AID-ANR18>3.0.CO;2-P
- Issue published online: 2 APR 2001
- Article first published online: 2 APR 2001
- Manuscript Accepted: 30 AUG 1999
- Manuscript Received: 1 FEB 1999
- Ministero Pubblica Istruzione
- Progetti 40% and 60%
- NIH. Grant Number: AR-40908
To investigate the in vitro ability of antiphospholipid antibodies (aPL) to bind human trophoblast cells and to affect gonadotropin secretion and invasiveness.
Antiphospholipid antibody IgG from women with recurrent miscarriages, β2-glycoprotein I (β2GPI)–independent IgG aPL human monoclonal antibody (mAb)(519), and IgM anti-β2GPI human mAb (TM1G2) were investigated for their binding to trophoblasts cultured for various amounts of time, their ability to affect invasiveness of Matrigel-coated filters, and their release of human chorionic gonadotropin (hCG).
Polyclonal IgG aPL, as well as mAb 519 and TM1G2, bound to trophoblasts, the highest binding being found when cells displayed the greatest amount of syncytium formation. TM1G2 binding was found to be β2GPI dependent. Both polyclonal and monoclonal aPL, but not the controls, significantly reduced hCG release and Matrigel invasiveness.
These findings suggest that aPL recognition of both anionic PL and adhered β2GPI on trophoblast cell structures might represent a potential pathogenetic mechanism for defective placentation in women with the antiphospholipid syndrome.