Updating on the pathogenic mechanisms 5 of the antiphospholipid antibodies-associated pregnancy loss

Research output: Contribution to journalArticle

Abstract

Anti-phospholipid antibodies (aPL) are risk factor for recurrent pregnancy loss and obstetrical complications. The mechanisms of aPL-mediated pregnancy failure are still a matter of research. Although aPL are associated with thrombosis, thrombotic events cannot explain all the miscarriages. There is evidence for a direct in vitro aPL effect on the trophoblast as shown by their binding; reduction of proliferation, human chorionic gonadotrophin release, in vitro invasiveness, adhesion molecule expression; and increased apoptosis. Such a direct reactivity is supported by the expression of beta2 glycoprotein (β2GP) I on trophoblast cell membranes. aPL/anti-β2GPI antibodies also bind to human decidual/endometrial cells in vitro and induce a pro-inflammatory phenotype. APL-mediated inflammatory processes at the placental level are apparently responsible for fetal loss at least in animal models. Both complement activation and pro-inflammatory cytokine/chemokine secretion have been shown to play a role. More recently, complement-induced tissue factor expression on infiltrating neutrophils was described as an additional pathogenic mechanisms mediated by aPL. As a whole, these findings do suggest that aPL may induce a defective placentation by acting at different levels without involving necessarily thrombotic events.

Original languageEnglish
Pages (from-to)332-337
Number of pages6
JournalClinical Reviews in Allergy and Immunology
Volume34
Issue number3
DOIs
Publication statusPublished - Jun 2008

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Keywords

  • Anti-phospholipid antibodies
  • Beta2 glycoprotein I
  • Complement
  • Cytokines
  • Decidual cells
  • Pregnancy loss
  • Trophoblast

ASJC Scopus subject areas

  • Immunology and Allergy

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