The associations of antiphospholipid antibodies (aPL) with thrombosis and f
etal death are well recognized, but the mechanism(s) that induce their prod
uction are not. We demonstrated induction of pathogenic aPL antibodies by i
mmunization with foreign beta(2)-GPI, or synthetic peptides representing th
e PL-binding site of the beta(2)-GPI. These antibodies caused intrauterine
fetal death and transverse myelopathy due to spinal cord infarction in mice
, and activated endothelial cells ill vitro. We also induced aPL in mice by
immunization with PL-binding viral peptides and observed their pathogenic
effects. This study demonstrated the pathogenic effects of aPL antibodies i
nduced by immunization with a human CMV-derived PL-binding synthetic peptid
e. We hypothesize that in APS patients aPL is induced by beta(2)-GPI-like P
L-binding products of human common bacteria or viruses. (C) 2000 Academic P
ress.