Human Reproduction, Vol. 11, No. 11, pp. 2408-2411, 1996
© 1996 European Society of Human Reproduction and Embryology
research-article |
Immunology: Defective maternalfetal interaction in a murine autoimmune model
1Department of Immunology, The Weizmann Institute of Science Rehovot 76100 Israel 2Experimental Immunology Branch, National Cancer Institute, National Institute of Health (NIH) Bethesda, MD 20892, USA
Correspondence: 3To whom correspondence should be addressed
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 pseudo-pregnant 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 embryonic compartments were defective, as a result of previous exposure to the ACA.
Key words: anti-cardiolipin antibodies/anti-phospholipid syndrome/autoimmunity/embryonic implantation/pregnancy
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