Abstract :
Anti-phospholipid syndrome (APS), recognised for less than 20 years, is one of the most diverse systemic autoimmune diseases. Recently, two groups have accumulated data showing that this disease is infectiously induced and molecular mimicry between infecting agents and the β-2-glycoprotein-1 (the autoantigen) might be the underlying mechanism. The multi-systemic manifestations (recurrent thrombo-embolic phenomena, repeated fetal loss, skin, valve and central nervous system involvement) can be explained by a panoply of pathogenetic mechanisms (hypercoagulation, anti-cytokines and hormonal effects) entailing two new aspects, that is, complement activation and binding to a natural anti-coagulant annexin V.
