Regulation of the complement system and immunological tolerance in pregnancy.
Apoptosis
Complement
Inflammation
Preeclampsia
Pregnancy
Tolerance
Journal
Seminars in immunology
ISSN: 1096-3618
Titre abrégé: Semin Immunol
Pays: England
ID NLM: 9009458
Informations de publication
Date de publication:
10 2019
10 2019
Historique:
received:
04
06
2019
accepted:
24
10
2019
pubmed:
24
11
2019
medline:
5
6
2020
entrez:
24
11
2019
Statut:
ppublish
Résumé
Preeclampsia is a serious vascular complication of the human pregnancy, whose etiology is still poorly understood. In preeclampsia, exacerbated apoptosis and fragmentation of the placental tissue occurs due to developmental qualities of the placental trophoblast cells and/or mechanical and oxidative distress to the syncytiotrophoblast, which lines the placental villi. Dysregulation of the complement system is recognized as one of the mechanisms of the disease pathology. Complement has the ability to promote inflammation and facilitate phagocytosis of placenta-derived particles and apoptotic cells by macrophages. In preeclampsia, an overload of placental cell damage or dysregulated complement system may lead to insufficient clearance of apoptotic particles and placenta-derived debris. Excess placental damage may lead to sequestration of microparticles, such as placental vesicles, to capillaries in the glomeruli of the kidney and other vulnerable tissues. This phenomenon could contribute to the manifestations of typical diagnostic symptoms of preeclampsia: proteinuria and new-onset hypertension. In this review we propose that the complement system may serve as a regulator of the complex tolerance and clearance processes that are fundamental in healthy pregnancy. It is therefore recommended that further research be conducted to elucidate the interactions between components of the complement system and immune responses in the context of complicated and healthy pregnancy.
Identifiants
pubmed: 31757607
pii: S1044-5323(19)30037-5
doi: 10.1016/j.smim.2019.101337
pii:
doi:
Substances chimiques
Receptors, Complement
0
Complement System Proteins
9007-36-7
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
101337Informations de copyright
Copyright © 2019 The Authors. Published by Elsevier Ltd.. All rights reserved.