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Manipulating CD4+ T Cell Pathways to Prevent Preeclampsia

Preeclampsia (PreE) is a placental disorder characterized by hypertension (HTN), proteinuria, and oxidative stress. Individuals with PreE and their children are at an increased risk of serious short- and long-term complications, such as cardiovascular disease, end-organ failure, HTN, neurodevelopmen...

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Autores principales: Murray, Eileen J., Gumusoglu, Serena B., Santillan, Donna A., Santillan, Mark K.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8789650/
https://www.ncbi.nlm.nih.gov/pubmed/35096797
http://dx.doi.org/10.3389/fbioe.2021.811417
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author Murray, Eileen J.
Gumusoglu, Serena B.
Santillan, Donna A.
Santillan, Mark K.
author_facet Murray, Eileen J.
Gumusoglu, Serena B.
Santillan, Donna A.
Santillan, Mark K.
author_sort Murray, Eileen J.
collection PubMed
description Preeclampsia (PreE) is a placental disorder characterized by hypertension (HTN), proteinuria, and oxidative stress. Individuals with PreE and their children are at an increased risk of serious short- and long-term complications, such as cardiovascular disease, end-organ failure, HTN, neurodevelopmental disorders, and more. Currently, delivery is the only cure for PreE, which remains a leading cause of morbidity and mortality among pregnant individuals and neonates. There is evidence that an imbalance favoring a pro-inflammatory CD4+ T cell milieu is associated with the inadequate spiral artery remodeling and subsequent oxidative stress that prime PreE’s clinical symptoms. Immunomodulatory therapies targeting CD4+ T cell mechanisms have been investigated for other immune-mediated inflammatory diseases, and the application of these prevention tactics to PreE is promising, as we review here. These immunomodulatory therapies may, among other things, decrease tumor necrosis factor alpha (TNF-α), cytolytic natural killer cells, reduce pro-inflammatory cytokine production [e.g. interleukin (IL)-17 and IL-6], stimulate regulatory T cells (Tregs), inhibit type 1 and 17 T helper cells, prevent inappropriate dendritic cell maturation, and induce anti-inflammatory cytokine action [e.g. IL-10, Interferon gamma (IFN-γ)]. We review therapies including neutralizing monoclonal antibodies against TNF-α, IL-17, IL-6, and CD28; statins; 17-hydroxyprogesterone caproate, a synthetic hormone; adoptive exogenous Treg therapy; and endothelin-1 pathway inhibitors. Rebalancing the maternal inflammatory milieu may allow for proper spiral artery invasion, placentation, and maternal tolerance of foreign fetal/paternal antigens, thereby combatting early PreE pathogenesis.
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spelling pubmed-87896502022-01-27 Manipulating CD4+ T Cell Pathways to Prevent Preeclampsia Murray, Eileen J. Gumusoglu, Serena B. Santillan, Donna A. Santillan, Mark K. Front Bioeng Biotechnol Bioengineering and Biotechnology Preeclampsia (PreE) is a placental disorder characterized by hypertension (HTN), proteinuria, and oxidative stress. Individuals with PreE and their children are at an increased risk of serious short- and long-term complications, such as cardiovascular disease, end-organ failure, HTN, neurodevelopmental disorders, and more. Currently, delivery is the only cure for PreE, which remains a leading cause of morbidity and mortality among pregnant individuals and neonates. There is evidence that an imbalance favoring a pro-inflammatory CD4+ T cell milieu is associated with the inadequate spiral artery remodeling and subsequent oxidative stress that prime PreE’s clinical symptoms. Immunomodulatory therapies targeting CD4+ T cell mechanisms have been investigated for other immune-mediated inflammatory diseases, and the application of these prevention tactics to PreE is promising, as we review here. These immunomodulatory therapies may, among other things, decrease tumor necrosis factor alpha (TNF-α), cytolytic natural killer cells, reduce pro-inflammatory cytokine production [e.g. interleukin (IL)-17 and IL-6], stimulate regulatory T cells (Tregs), inhibit type 1 and 17 T helper cells, prevent inappropriate dendritic cell maturation, and induce anti-inflammatory cytokine action [e.g. IL-10, Interferon gamma (IFN-γ)]. We review therapies including neutralizing monoclonal antibodies against TNF-α, IL-17, IL-6, and CD28; statins; 17-hydroxyprogesterone caproate, a synthetic hormone; adoptive exogenous Treg therapy; and endothelin-1 pathway inhibitors. Rebalancing the maternal inflammatory milieu may allow for proper spiral artery invasion, placentation, and maternal tolerance of foreign fetal/paternal antigens, thereby combatting early PreE pathogenesis. Frontiers Media S.A. 2022-01-12 /pmc/articles/PMC8789650/ /pubmed/35096797 http://dx.doi.org/10.3389/fbioe.2021.811417 Text en Copyright © 2022 Murray, Gumusoglu, Santillan and Santillan. https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Bioengineering and Biotechnology
Murray, Eileen J.
Gumusoglu, Serena B.
Santillan, Donna A.
Santillan, Mark K.
Manipulating CD4+ T Cell Pathways to Prevent Preeclampsia
title Manipulating CD4+ T Cell Pathways to Prevent Preeclampsia
title_full Manipulating CD4+ T Cell Pathways to Prevent Preeclampsia
title_fullStr Manipulating CD4+ T Cell Pathways to Prevent Preeclampsia
title_full_unstemmed Manipulating CD4+ T Cell Pathways to Prevent Preeclampsia
title_short Manipulating CD4+ T Cell Pathways to Prevent Preeclampsia
title_sort manipulating cd4+ t cell pathways to prevent preeclampsia
topic Bioengineering and Biotechnology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8789650/
https://www.ncbi.nlm.nih.gov/pubmed/35096797
http://dx.doi.org/10.3389/fbioe.2021.811417
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