Pathogenesis of the Antiphospholipid Syndrome
- Antiphospholipid antibodies (aPL) are both diagnostic markers and pathogenic drivers for the antiphospholipid syndrome.
- β2 glycoprotein I-dependent autoantibodies seem to be the main pathogenic subpopulation of aPL.
Meroni PL, Borghi MO, Raschi E, Tedesco F
Pathogenesis of antiphospholipid syndrome: understanding the antibodies
Nat. Rev. Rheumatol. 2011; 7: 330-339
Background: Antiphospholipid syndrome (APS) is characterized by vascular thrombosis and/or pregnancy morbidity, in association with antiphospholipid antibodies (aPL). Detectable by anticardiolipin, anti-β2 glycoprotein I and lupus anticoagulant assays, aPL are not only diagnostic of APS but are also believed to have a pathogenic role, mediating several clinical manifestations of the syndrome.
Conclusions: Although APS is considered as a single disease, there seem to be slightly different mechanisms for the two clinical manifestations of APS, thrombosis and pregnancy morbidity. Thrombosis does not seem to have sole responsibility for the obstetrical complications. The three aPL subtypes (anticardiolipin, anti-ß2GPI and lupus anticoagulant) detect slightly different populations. Whether different subpopulations of autoantibodies, detected by the same diagnostic assays, are responsible for the different clinical manifestations remains an open question.
Comment: Pier Luigi Meroni et al. published this review on the pathogenesis of the antiphospholipid syndrome (APS) in Nature Reviews / Rheumatology in June this year. This article is the most comprehensive and summarizing review on this matter in the last years and is worth to read for everybody interested in autoimmunity and in particular in APS. It is available with free access online (http://www.nature.com/nrrheum/journal/v7/n6/full/nrrheum.2011.52.html).
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