Infections and vaccines in the etiology of antiphospholipid syndrome

Purpose of review To present scientific evidence supporting the infectious origin for the antiphospholipid syndrome (APS) by molecular mimicry between pathogens, infection and vaccination with beta 2-glycoprotein I (beta 2-GPI) molecule. Recent findings APS is characterized by the presence of pathogenic autoantibodies against beta 2-GPI. The infection etiology of APS was well established. Likewise, a link between vaccination such as tetanus toxoid may trigger antibodies targeting tetanus toxoid and beta 2-GPI, due to molecular mimicry between the two molecules. During the years, the pathogenic potential of anti-tetanus toxoid antibodies cross reactive with beta 2-GPI were found to be pathogenic in animal models, inducing experimental APS. Summary Accumulated evidence supports that the presence of anti-beta 2-GPI antibodies is associated with a history of infections and the main mechanism to explain this correlation is molecular mimicry. The relationship between tetanus toxoid vaccination and APS reveals a novel view on the autoimmune/autoinflammatory syndrome induced by adjuvants (ASIA).