Infections and vaccines in the etiology of antiphospholipid syndrome

Paola Cruz-Tapias, Miri Blank, Juan Manuel Anaya, Yehuda Shoenfeld

Resultado de la investigación: Contribución a RevistaRevisión Literaria

33 Citas (Scopus)

Resumen

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.
Idioma originalEnglish (US)
Páginas (desde-hasta)389-393
Número de páginas5
PublicaciónCurrent Opinion in Rheumatology
DOI
EstadoPublished - jul 1 2012

Huella dactilar

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

Citar esto

Cruz-Tapias, Paola ; Blank, Miri ; Anaya, Juan Manuel ; Shoenfeld, Yehuda. / Infections and vaccines in the etiology of antiphospholipid syndrome. En: Current Opinion in Rheumatology. 2012 ; pp. 389-393.
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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). {\circledC} 2012 Wolters Kluwer Health | Lippincott Williams & Wilkins.",
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Infections and vaccines in the etiology of antiphospholipid syndrome. / Cruz-Tapias, Paola; Blank, Miri; Anaya, Juan Manuel; Shoenfeld, Yehuda.

En: Current Opinion in Rheumatology, 01.07.2012, p. 389-393.

Resultado de la investigación: Contribución a RevistaRevisión Literaria

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AU - Anaya, Juan Manuel

AU - Shoenfeld, Yehuda

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N2 - 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.

AB - 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.

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