Infections and vaccines in the etiology of antiphospholipid syndrome Review

abstract

  • 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). © 2012 Wolters Kluwer Health | Lippincott Williams & Wilkins.

publication date

  • 2012/7/1

keywords

  • Animal Models
  • Antibodies
  • Antiphospholipid Syndrome
  • Autoantibodies
  • Glycoproteins
  • Health
  • Infection
  • Molecular Mimicry
  • Tetanus Toxoid
  • Vaccination
  • Vaccines

International Standard Serial Number (ISSN)

  • 1040-8711

number of pages

  • 5

start page

  • 389

end page

  • 393