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Immunology of Pregnancy

Editor(s): Markert U.R. (Jena) 
Cover

Immunology of Preeclampsia

Matthiesen L.a · Berg G.a · Ernerudh J.b · Ekerfelt C.b · Jonsson Y.b · Sharma S.c

Author affiliations

aDepartment of Molecular and Clinical Medicine, Division of Obstetrics and Gynaecology and b Department of Molecular and Clinical Medicine, Division of Clinical Immunology, University Hospital, Linkoping, Sweden; cDepartment of Pediatrics and Pathology, Women and Infants Hospital of Rhode Island, Brown University, Providence, R.I., USA

Related Articles for ""

Markert UR (ed): Immunology of Pregnancy. Chem Immunol Allergy. Basel, Karger, 2005, vol 89, pp 49-61

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Article / Publication Details

First-Page Preview
Abstract of Paper

Published online: August 25, 2005
Cover Date: 2005

Number of Print Pages: 13
Number of Figures: 0
Number of Tables: 0

ISBN: 978-3-8055-7970-4 (Print)
eISBN: 978-3-318-01248-4 (Online)

Abstract

Preeclampsia is a placenta-dependent disorder with both local and systemic anomalies with neonatal and maternal morbidity. It is manifested late in pregnancy, but the onset is during early stages of gestation. The current hypothesis regarding the aetiology of preeclampsia is focused on maladaptation of immune responses and defective trophoblast invasion. Thus, an excessive maternal inflammatory response, perhaps directed against foreign fetal antigens, results in a chain of events including shallow trophoblast invasion, defective spiral artery remodelling, placental infarction and release of pro-inflammatory cytokines and placental fragments in the systemic circulation. During normal pregnancy, trophoblasts interact in the decidua with the unique uterine NK cells, modifying their cytokine repertoire, regulating adhesion molecules and matrix metalloproteinases. The inability of trophoblasts to accomplish these changes might be a critical factor for the onset of preeclampsia. Several cytokines, produced at the maternal-fetal interface, have an impact on trophoblast invasion. It is suggested that deficiency of interleukin-10 may contribute to enhanced inflammatory responses towards the trophoblasts elicited by e.g. tumour necrosis factor-α and interferon-γ. Consequently, trophoblasts subjected to a high rate of apoptosis are hampered in their invasive capacity resulting in defective transformation of spiral arteries, hypoxia, thrombosis and infarction of the placenta. The ensuing infarction of placenta leads to leakage of increasing amounts of placental fragments and cytokines in the maternal circulation and an exaggerated systemic endothelial activation as identified in preeclampsia. So far, treatment of preeclampsia is focused on signs like hypertension, whereas attempts of modifying immune responses may be a possibility in the future.


Article / Publication Details

First-Page Preview
Abstract of Paper

Published online: August 25, 2005
Cover Date: 2005

Number of Print Pages: 13
Number of Figures: 0
Number of Tables: 0

ISBN: 978-3-8055-7970-4 (Print)
eISBN: 978-3-318-01248-4 (Online)


Copyright / Drug Dosage / Disclaimer

Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher.
Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug.
Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.