The origin of the antiphospholipid antibodies and mechanisms involved in th
eir production in patients with the antiphospholipid syndrome is not unders
tood. The authors hypothesize that incidental exposure to phospholipid-bind
ing viral or bacterial products that have structural similarity to the phos
pholipid binding site of beta (2)-glycoprotein I and like this protein can
bind to phospholipids and may trigger the antiphospholipid antibody product
ion in these patients. As a support for this hypothesis the authors describ
e production of pathogenic antiphospholipid antibodies in normal mice by im
munization with a synthetic phospholipid-binding viral peptide that has seq
uence similarity with beta (2)-glycoprotein I (molecular mimicry).