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

Infections and vaccines in the etiology of antiphospholipid syndrome.

Author information

1
Zabludowitz Center for Autoimmune Diseases, Sheba Medical Center affiliated to Sackler Faculty of Medicine, Tel-Aviv University, Israel.

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).

PMID:
22617823
DOI:
10.1097/BOR.0b013e32835448b8
[Indexed for MEDLINE]

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