The annexin A5 protective shield model revisited: inherited carriage of the M2/ANXA5 haplotype in placenta as a predisposing factor for the development of obstetric antiphospholipid antibodies

• Published in: Lupus Vol. 21; no. 7; pp. 796 - 798
• Main Authors: Bogdanova, N, Baleva, M, Kremensky, I, Markoff, A
• Format: Journal Article
• Language: English
• Published: London, England SAGE Publications 01.06.2012; Sage Publications Ltd
• Subjects: Annexin A5 - genetics; Annexin A5 - metabolism; Annexins; Antibodies; Anticoagulants; Antigenic determinants; antiphospholipid antibodies; antiphospholipid syndrome; Antiphospholipid Syndrome - genetics; Antiphospholipid Syndrome - immunology; Antiphospholipid Syndrome - metabolism; Biochemistry; Female; Haplotypes; Humans; Hypotheses; Lupus; Obstetrics; Patients; Placenta; Placenta - metabolism; Preeclampsia; Pregnancy; Pregnancy Complications - genetics; Pregnancy Complications - immunology; Pregnancy Complications - metabolism; Proteins; Reviews; thrombophilia; Bulgaria; Germany; annexin A5; M2/ANXA5; aPL; aPS; ANXA5; obstetric APS
• ISSN: 0961-2033; 1477-0962
• DOI: 10.1177/0961203312438235

This concise review summarizes the role of reduced ANXA5 expression through carriage of the M2/ANXA5 haplotype as a predisposing factor for various thrombophilia related obstetric complications. A revised ANXA5 ‘protective shield’ model is emphasized, where decreased coverage resulting of M2 carriage at placental villi could lead directly to the observed pathology and on the other hand through exposing of antiphospholipid antigenic determinants, to the development of antiphospholipid antibodies (aPL). The aPL then can further disrupt the ANXA5 protective shield. Available and prospective evidence for this revised model is discussed. Conclusions are made about the diagnostic implications of M2 carriage and possible therapeutic strategies with anticoagulants, proven successful in obstetric antiphospholipid syndrome (APS) treatment.