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Current Opinion In Rheumatology • July 2012<br />

Infections and vaccines<br />

in the etiology of antiphospholipid syndrome<br />

Author information<br />

Cruz-Tapias P1, Blank M, Anaya JM, Shoenfeld Y.<br />

Zabludowitz Center for Autoimmune Diseases<br />

Sheba Medical Center affiliated to Sackler Faculty of Medicine<br />

Tel-Aviv University, Israel<br />

Abstract<br />

PURPOSE OF REVIEW<br />

To present scientific evidence supporting the infectious origin for the antiphospholipid<br />

syndrome (APS) by molecular mimicry between pathogens,<br />

infection and vaccination with ß2-glycoprotein I (ß2-GPI) molecule.<br />

RECENT FINDINGS<br />

APS is characterized by the presence of pathogenic autoantibodies against<br />

ß2-GPI. The infection etiology of APS was well established. Likewise, a<br />

link between vaccination such as tetanus toxoid may trigger antibodies<br />

targeting tetanus toxoid and ß2-GPI, due to molecular mimicry between<br />

the two molecules. During the years, the pathogenic potential of anti-tetanus<br />

toxoid antibodies cross reactive with ß2-GPI were found to be pathogenic<br />

in animal models, inducing experimental APS.<br />

“The relationship between tetanus toxoid vaccination<br />

and Anti-Phospholipid Syndrome reveals a novel view<br />

on the autoimmune/autoinflammatory syndrome<br />

induced by adjuvants (ASIA).<br />

SUMMARY<br />

Accumulated evidence supports that the presence of anti-ß2-GPI antibodies<br />

is associated with a history of infections and the main mechanism to<br />

explain this correlation is molecular mimicry. The relationship between<br />

tetanus toxoid vaccination and APS reveals a novel view on the autoimmune/autoinflammatory<br />

syndrome induced by adjuvants (ASIA).<br />

http://www.ncbi.nlm.nih.gov/pubmed/?term=22617823

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