Preeclampsia—an immune disease? An epidemiologic narrative
The maternal syndrome preeclampsia is triggered by syncytiotrophoblast (STB) stress; the heterogeneity of the syndrome is caused by the different pathways leading to this STB stress. Inflammation plays a pivotal role in the pathogenesis of preeclampsia. While, the immune system at large is therefore...
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Format: | Article |
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Open Exploration Publishing Inc.
2021-12-01
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Series: | Exploration of Immunology |
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Online Access: | https://www.explorationpub.com/Journals/ei/Article/100322 |
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author | Gustaaf Albert Dekker Pierre Yves Robillard |
author_facet | Gustaaf Albert Dekker Pierre Yves Robillard |
author_sort | Gustaaf Albert Dekker |
collection | DOAJ |
description | The maternal syndrome preeclampsia is triggered by syncytiotrophoblast (STB) stress; the heterogeneity of the syndrome is caused by the different pathways leading to this STB stress. Inflammation plays a pivotal role in the pathogenesis of preeclampsia. While, the immune system at large is therefore intimately involved in the causation of this heterogeneous syndrome, the role of the adaptive immune system is more controversial. The classic paradigm placed preeclampsia as the disease of the nulliparous pregnant women. Up to the later part of the 20th century, human reproduction, particularly in Western societies, was characterised by a low rate of pre-marital sex, and the great majority of children being born within one stable sexual relationship. More prolonged periods of regular sexual intercourse within a stable relationship have been demonstrated to reduce the risk of preeclampsia and fetal growth restriction. Primarily animal studies have indeed shown that repetitive sperm exposure leads to partner specific mucosal tolerance. Societal changes made partner change over the reproductive period of individual women extremely common. For the adaptive immune system of multiparous women, being pregnant in a new sexual relationship (primipaternity) would represent being faced with a new “hemi-allograft”. In these pregnancies, potential couple-specific immune “maladaptation” could lead to the superficial cytotrophoblast invasion of the spiral arteries, known to be associated with early-onset preeclampsia. Having a new pregnancy in a different relationship does indeed increase the risk for this type of preeclampsia. Large epidemiologic population studies identified prolonged birth interval but not “primipaternity” as a risk factor for preeclampsia in multiparous women. This apparent contradiction is explained by the fact that the great majority of preeclampsia cases in these population studies involve term preeclampsia. In late-onset preeclampsia, the far more common phenotype of the syndrome, STB stress is not caused by lack of proper spiral artery modification, but involves maternal genetic predisposition to cardiovascular and metabolic disease, with in particular obesity/metabolic syndrome representing major players. Partner or couple specific issues are not detectable in this disease phenotype. |
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institution | Directory Open Access Journal |
issn | 2768-6655 |
language | English |
last_indexed | 2024-12-22T20:06:14Z |
publishDate | 2021-12-01 |
publisher | Open Exploration Publishing Inc. |
record_format | Article |
series | Exploration of Immunology |
spelling | doaj.art-eaa993e48f5242b7b677c73a2489d2382022-12-21T18:14:07ZengOpen Exploration Publishing Inc.Exploration of Immunology2768-66552021-12-011532534010.37349/ei.2021.00022Preeclampsia—an immune disease? An epidemiologic narrativeGustaaf Albert Dekker0https://orcid.org/0000-0002-7362-6683Pierre Yves Robillard1https://orcid.org/0000-0001-8916-9045University of Adelaide, Women’s and Children’s Division Northern Adelaide Local Health Network Elizabeth Vale, SA 5112, AustraliaNeonatology, Centre Hospitalier Universitaire Sud-Reunion, BP 350, 97448 Saint-Pierre cedex, Reunion, France; Centre d’études périnatales Océan-Indien (CEPOI). Centre Hospitalier Universitaire Sud-Reunion, BP 350, 97448, Saint-Pierre cedex, Reunion, FranceThe maternal syndrome preeclampsia is triggered by syncytiotrophoblast (STB) stress; the heterogeneity of the syndrome is caused by the different pathways leading to this STB stress. Inflammation plays a pivotal role in the pathogenesis of preeclampsia. While, the immune system at large is therefore intimately involved in the causation of this heterogeneous syndrome, the role of the adaptive immune system is more controversial. The classic paradigm placed preeclampsia as the disease of the nulliparous pregnant women. Up to the later part of the 20th century, human reproduction, particularly in Western societies, was characterised by a low rate of pre-marital sex, and the great majority of children being born within one stable sexual relationship. More prolonged periods of regular sexual intercourse within a stable relationship have been demonstrated to reduce the risk of preeclampsia and fetal growth restriction. Primarily animal studies have indeed shown that repetitive sperm exposure leads to partner specific mucosal tolerance. Societal changes made partner change over the reproductive period of individual women extremely common. For the adaptive immune system of multiparous women, being pregnant in a new sexual relationship (primipaternity) would represent being faced with a new “hemi-allograft”. In these pregnancies, potential couple-specific immune “maladaptation” could lead to the superficial cytotrophoblast invasion of the spiral arteries, known to be associated with early-onset preeclampsia. Having a new pregnancy in a different relationship does indeed increase the risk for this type of preeclampsia. Large epidemiologic population studies identified prolonged birth interval but not “primipaternity” as a risk factor for preeclampsia in multiparous women. This apparent contradiction is explained by the fact that the great majority of preeclampsia cases in these population studies involve term preeclampsia. In late-onset preeclampsia, the far more common phenotype of the syndrome, STB stress is not caused by lack of proper spiral artery modification, but involves maternal genetic predisposition to cardiovascular and metabolic disease, with in particular obesity/metabolic syndrome representing major players. Partner or couple specific issues are not detectable in this disease phenotype.https://www.explorationpub.com/Journals/ei/Article/100322preeclampsia heterogeneous syndromeadaptive immune systemearly-onset preeclampsia |
spellingShingle | Gustaaf Albert Dekker Pierre Yves Robillard Preeclampsia—an immune disease? An epidemiologic narrative Exploration of Immunology preeclampsia heterogeneous syndrome adaptive immune system early-onset preeclampsia |
title | Preeclampsia—an immune disease? An epidemiologic narrative |
title_full | Preeclampsia—an immune disease? An epidemiologic narrative |
title_fullStr | Preeclampsia—an immune disease? An epidemiologic narrative |
title_full_unstemmed | Preeclampsia—an immune disease? An epidemiologic narrative |
title_short | Preeclampsia—an immune disease? An epidemiologic narrative |
title_sort | preeclampsia an immune disease an epidemiologic narrative |
topic | preeclampsia heterogeneous syndrome adaptive immune system early-onset preeclampsia |
url | https://www.explorationpub.com/Journals/ei/Article/100322 |
work_keys_str_mv | AT gustaafalbertdekker preeclampsiaanimmunediseaseanepidemiologicnarrative AT pierreyvesrobillard preeclampsiaanimmunediseaseanepidemiologicnarrative |