Antiphospholipid antibodies and extracellular vesicles in pregnancy

Antiphospholipid antibodies (aPL) are autoantibodies that target phospholipid‐binding proteins, such as β2 glycoprotein I (β2GPI), and can induce thrombosis systemically, as well as increase the risk of obstetric complications such as recurrent miscarriage and preeclampsia. Due to the expression of...

Full description

Saved in:
Bibliographic Details
Published in:American journal of reproductive immunology (1989) 2021-02, Vol.85 (2), p.e13312-n/a
Main Authors: Tong, Mancy, Tsai, Bridget W., Chamley, Lawrence W.
Format: Article
Language:English
Subjects:
alarmin
Antiphospholipid antibodies
Autoantibodies
DAMP
danger signal
exosome
Extracellular vesicles
Fetuses
Glycoprotein I
microparticle
misfolded proteins
mitochondria
Obstetrics
Phospholipids
Placenta
Pre-eclampsia
Pregnancy
SLE
Thrombosis
Trophoblasts
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Antiphospholipid antibodies (aPL) are autoantibodies that target phospholipid‐binding proteins, such as β2 glycoprotein I (β2GPI), and can induce thrombosis systemically, as well as increase the risk of obstetric complications such as recurrent miscarriage and preeclampsia. Due to the expression of β2GPI by placental trophoblasts, aPL readily target the maternal‐fetal interface during pregnancy and many studies have investigated the deleterious effects of aPL on placental trophoblast function. This review will focus on studies that have examined the effects of aPL on the production and modification of extracellular vesicles (EVs) from trophoblasts, as EVs are a key mode of feto‐maternal communication in both normal and pathological pregnancy. A more comprehensive understanding of the effects of aPL on the quantity and cargo of EVs extruded by the human placenta may contribute to our current knowledge of how aPL induce both systemic and obstetric disease.
ISSN:1046-7408
1600-0897
DOI:10.1111/aji.13312