Journal
CURRENT OPINION IN RHEUMATOLOGY
Volume 24, Issue 4, Pages 389-393Publisher
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/BOR.0b013e32835448b8
Keywords
beta 2-glycoprotein I; antiphospholipid syndrome; tetanus toxoid
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Funding
- Federico Foundation
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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).
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