The clinical associations of antiphospholipid antibodies (aPL) are wel
l recognized but the mechanism(s) causing the production of these anti
bodies are not yet known. We demonstrated the induction of pathogenic
aPL antibodies that caused intrauterine fetal death and transverse mye
lopathy due to spinal cord infarction in mice by immunization with for
eign beta(2)GPI. We also induced aPL and anti-beta(2)-GPI in mice by i
mmunization with PL-binding viral peptides and hypothesized that in AP
S patients, aPL may be induced by beta(2)GPI-like-PL-binding products
of common human bacteria and viruses.