Defective maternal-fetal interaction in a murine autoimmune model

Boris Tartakovsky, Bonnie L. Bermas, Zev Sthoeger, Gene M. Shearer, Edna Mozes

Research output: Contribution to journalArticlepeer-review

40 Scopus citations


Anti-cardiolipin antibodies (ACA) are associated with recurrent fetal loss, but their role in this pathological condition is unknown. We recently developed an experimental mouse model of the anti-phospholipid syndrome, in which immunization of female mice with a monoclonal anti-cardiolipin antibody resulted in substantial failure of pregnancy. We observed that pre-implantation embryos derived from ACA-injected mothers exhibited morphological abnormalities and failed to implant in vitro. In the present study, we designed embryo transfer experiments to determine whether defective embryonic development originated as a maternal defect, an embryonic defect or both. Embryos (3.5 day old), taken from ACA- and control-immunized mothers were transferred into either an ACA- or a control-treated uterine environment (day 2.5 pseudopregnant females). On day 14 of gestation the incidence of pregnancy, the average number of fetuses per female and fetal resorptions were assessed. The ACA-treated uterine environment was found to be non-supportive for the development and implantation of normal embryos. Moreover, embryos derived from ACA-immunized mothers, even after their removal from the ACA-environment and transfer to a normal uterus, remained deficient. These results demonstrate that both the maternal and the ernbryonic compartments were defective, as a result of previous exposure to the ACA.

Original languageEnglish (US)
Pages (from-to)2408-2411
Number of pages4
JournalHuman Reproduction
Issue number11
StatePublished - Nov 1996


  • Anti-cardiolipin antibodies
  • Anti-phospholipid syndrome
  • Autoimmunity
  • Embryonic implantation
  • Pregnancy

ASJC Scopus subject areas

  • Reproductive Medicine
  • Obstetrics and Gynecology


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