Anti-cardiolipin antibodies (ACA) are associated with recurrent fetal
loss, but their role in this pathological condition is unknown, Ne rec
ently developed an experimental mouse model of the anti-phospholipid s
yndrome, in which immunization of female mise with a monoclonal anti-c
ardiolipin antibody resulted in substantial failure of pregnancy We ob
served 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 deter
mine 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 AC
A- or a control-treated uterine environment (day 2.5 pseudo-pregnant f
emales). On day 14 of gestation the incidence of pregnancy, the averag
e number of fetuses per female and fetal resorptions were assessed, Th
e ACA-treated uterine environment was found to be non-supportive for t
he development and implantation of normal embryos, Moreover, embryos d
erived from ACA-immunized mothers, even after their removal from the A
CA-environment and transfer to a normal uterus, remained deficient, Th
ese results demonstrate that both the maternal and the embryonic compa
rtments were defective, as a result of previous exposure to the ACA.