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Open AccessJournal ArticleDOI

Immunology of Pre-Eclampsia

TLDR
In this paper, the pathogenesis of pre-eclampsia can be related to defined immune mechanisms that are appropriate to the fetomaternal frontier, and the first pregnancy preponderance and partner specificity can be explained by this model.
Abstract
Pre-eclampsia develops in stages, only the last being the clinical illness This is generated by a non-specific, systemic (vascular), inflammatory response, secondary to placental oxidative stress and not by reactivity to fetal alloantigens However, maternal adaptation to fetal (paternal alloantigens) is crucial in the earlier stages A pre-conceptual phase involves maternal tolerization to paternal antigens by seminal plasma After conception, regulatory T cells, interacting with indoleamine 2,3-dioxygenase, together with decidual NK cell recognition of fetal HLA-C on extravillous trophoblast may facilitate placental growth by immunoregulation Complete failure of this mechanism would cause miscarriage, while partial failure would cause poor placentation and dysfunctional uteroplacental perfusion The first pregnancy preponderance and partner specificity of pre-eclampsia can be explained by this model For the first time, the pathogenesis of pre-eclampsia can be related to defined immune mechanisms that are appropriate to the fetomaternal frontier Now, the challenge is to prove the detail

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Citations
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BookDOI

Regulatory T Cells

TL;DR: Firm evidence is provided for Foxp3+CD25+CD4+ Treg cells as an indispensable cellular constituent of the normal immune system for establishing and maintaining immunologic self-tolerance and immune homeostasis.
Journal ArticleDOI

Pre-eclampsia part 1: current understanding of its pathophysiology

TL;DR: The diagnosis, classification, clinical manifestations and putative pathogenetic mechanisms of pre-eclampsia are discussed.
Journal ArticleDOI

The role of inflammation in the pathology of preeclampsia.

TL;DR: These studies show that restoring the balance of the immune system through increasing Tregs, either by adoptive transfer or by infusing IL-10, reduces the blood pressure and pathophysiology associated with placental ischaemia in pregnant rats.
Journal ArticleDOI

Spiral artery remodeling and trophoblast invasion in preeclampsia and fetal growth restriction: relationship to clinical outcome.

TL;DR: In this paper, the authors examined spiral artery remodeling and extravillous-cytotrophoblast in placental bed biopsies from normal pregnancy, preeclampsia, and severe FGR and compared with clinical parameters.
Journal ArticleDOI

Redefining preeclampsia using placenta-derived biomarkers.

TL;DR: The classic definitions of preeclampsia have become outdated and that the definition could be modernized to take account of the current understanding of disease pathophysiology, and a first step is proposed that incorporates the placental biomarker placenta growth factor (PlGF).
References
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Journal ArticleDOI

How regulatory T cells work.

TL;DR: The hypothesis that effector T cells may not be 'innocent' parties in this suppressive process and might in fact potentiate TReg-cell function is proposed.
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Prevention of allogeneic fetal rejection by tryptophan catabolism

TL;DR: In 1953 Medawar pointed out that survival of the genetically disparate (allogeneic) mammalian conceptus contradicts the laws of tissue transplantation and suppresses T cell activity and defends itself against rejection.
Journal ArticleDOI

Latest advances in understanding preeclampsia.

TL;DR: Recent work on the causes of preeclampsia is summarized, which reveals a new mode of maternal immune recognition of the fetus, relevant to the condition, and circulating factors derived from the placenta are now better understood.
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From endoplasmic-reticulum stress to the inflammatory response

TL;DR: New observations suggest that the unfolded-protein response can initiate inflammation, and the coupling of these responses in specialized cells and tissues is now thought to be fundamental in the pathogenesis of inflammatory diseases.
Journal ArticleDOI

Shedding microvesicles: artefacts no more

TL;DR: The small vesicles shed from the surface of many cells upon stimulation, considered for a long time to be artefacts, are now recognized as specific structures that are distinct from the exosomes released upon exocytosis of multivesicular bodies.
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