Infections and vaccines in the etiology of antiphospholipid syndrome

Paola Cruz-Tapias, Miri Blank, Juan Manuel Anaya, Yehuda Shoenfeld

Research output: Contribution to journalReview articlepeer-review

72 Scopus citations


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 β2-glycoprotein I (β2-GPI) molecule. Recent findings: APS is characterized by the presence of pathogenic autoantibodies against β2-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 β2-GPI, due to molecular mimicry between the two molecules. During the years, the pathogenic potential of anti-tetanus toxoid antibodies cross reactive with β2-GPI were found to be pathogenic in animal models, inducing experimental APS. Summary: Accumulated evidence supports that the presence of anti-β2-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).

Original languageEnglish (US)
Pages (from-to)389-393
Number of pages5
JournalCurrent Opinion in Rheumatology
Issue number4
StatePublished - Jul 2012

All Science Journal Classification (ASJC) codes

  • Rheumatology


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