title: Maternal autoimmune diseases and immunologically induced embryonic and fetoplacental damage.
abstract: BACKGROUND
  Autoimmune diseases are a group of illnesses in which autoantibodies are produced against various organs, presenting with a variety of clinical symptoms. In this review, we discuss the different aspects of autoimmune diseases in pregnancy. We also describe experimental models that help to understand the etiology and pathogenesis of the effects of this maternal disease on the developing embryo, fetus and placenta.
  
  
  METHODS
  The possible direct effects of sera or IgG obtained from women with systemic lupus erythematosus/antiphospholipid syndrome (SLE/APS) and recurrent pregnancy loss (RPL) were examined on cultured 10.5- and 11.5-day-old rat embryos and on cultured human placental explants, as compared to sera from healthy women or synthetic medium that were used as controls. In addition, we examined the effects of the sera obtained from these women after successful treatment that allowed the birth of normal infants.
  
  
  RESULTS
  We observed increased embryonic death and anomalies in embryos cultured on sera and IgG from SLE/APS women. Similarly, when human placental explants were cultured on these sera, trophoblastic cell growth was reduced and apoptotic rate was increased. Successful treatment also reduced the damage caused by the sera from these women in the cultured embryos and placentas.
  
  
  CONCLUSIONS
  Our results, and the cited studies, point to the important role of the placental damage in the etiology of RPL associated with SLE/APS. Animal models, both in vivo and in vitro, as well as cultured early human placental explants can be used successfully to understand some of the pathogenic aspects of SLE/APS and RPL.
authors.affiliation: Laboratory of Teratology, Department of Anatomy and Cell Biology, Hebrew University Hadassah Medical School, Jerusalem, Israel. ornoy@cc.huji.ac.il
authors.forename: Asher
authors.initials: A
authors.lastname: Ornoy
authors.forename: Limor
authors.initials: L
authors.lastname: Chen
authors.forename: Robert M
authors.initials: RM
authors.lastname: Silver
authors.forename: Richard K
authors.initials: RK
authors.lastname: Miller
mesh_terms: D000026:Abortion, Habitual / Q000209:etiology / Q000276:immunology; D000818:Animals; D017152:Antibodies, Antiphospholipid / Q000276:immunology; D000925:Anticoagulants / Q000627:therapeutic use; D016736:Antiphospholipid Syndrome / Q000150:complications / Q000188:drug therapy / Q000276:immunology; D001241:Aspirin / Q000627:therapeutic use; D001327:Autoimmune Diseases; D004195:Disease Models, Animal; D004622:Embryo, Mammalian / Q000002:abnormalities / Q000187:drug effects*; D005260:Female; D006493:Heparin / Q000627:therapeutic use; D006801:Humans; D007074:Immunoglobulin G / Q000276:immunology; D008180:Lupus Erythematosus, Systemic / Q000150:complications / Q000188:drug therapy / Q000276:immunology; D009924:Organ Culture Techniques; D010920:Placenta / Q000276:immunology / Q000378:metabolism / Q000473:pathology*; D010975:Platelet Aggregation Inhibitors / Q000627:therapeutic use; D011247:Pregnancy; D011248:Pregnancy Complications / Q000188:drug therapy / Q000276:immunology*; D011256:Pregnancy Outcome; D051381:Rats
chemical_list: D017152:Antibodies, Antiphospholipid; D000925:Anticoagulants; D007074:Immunoglobulin G; D010975:Platelet Aggregation Inhibitors; D006493:Heparin; D001241:Aspirin