Infections and vaccines in the etiology of antiphospholipid syndrome

Curr Opin Rheumatol. 2012 Jul;24(4):389-93. doi: 10.1097/BOR.0b013e32835448b8.


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).

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Adjuvants, Immunologic / adverse effects
  • Antiphospholipid Syndrome / etiology*
  • Antiphospholipid Syndrome / immunology
  • Autoantibodies / biosynthesis
  • Cross Reactions / immunology
  • Humans
  • Infections / complications*
  • Molecular Mimicry
  • Tetanus Toxoid / adverse effects*
  • beta 2-Glycoprotein I / immunology


  • Adjuvants, Immunologic
  • Autoantibodies
  • Tetanus Toxoid
  • beta 2-Glycoprotein I