The antiphospholipid syndrome (APS) is characterized by the presence of pathogenic autoantibodies against β2-glycoprotein-I (β2GPI) that can appear as a secondary complication to microbial infections, but the mechanisms involved remain unclear. In March 15 Journal of Clinical Investigation, Miri Blank and colleagues from Tel Aviv University show that bacterial peptides homologous to β2GPI may account for the infectious etiology of APS (J Clin Invest 2002, 109:797-804).

Blank et al. evaluated the APS-related pathogenic potential of microbial pathogens carrying sequences related to a hexapeptide (TLRVYK), recognized specifically by a pathogenic anti-β2GPI monoclonal antibody. They injected mice with extracts from a panel of microbial preparations and found high titers of antipeptide TLRVYK anti-β2GPI antibodies in mice immunized with Haemophilus influenzae, Neisseria gonorrhoeae, or tetanus toxoid. When naïve mice were infused with the affinity-purified antipeptide antibodies they showed substantial thrombocytopenia, prolonged activated partial tromboplastin time and elevated...