Mechanisms of immune regulation by the placenta: Role of type I interferon and interferon‐stimulated genes signaling during pregnancy

Pregnancy is a unique condition where the maternal immune system is continuously adapting in response to the stages of fetal development and signals from the environment. The placenta is a key mediator of the fetal/maternal interaction by providing signals that regulate the function of the maternal...

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Published inImmunological reviews Vol. 308; no. 1; pp. 9 - 24
Main Authors Ding, Jiahui, Maxwell, Anthony, Adzibolosu, Nicholas, Hu, Anna, You, Yuan, Liao, Aihua, Mor, Gil
Format Journal Article
LanguageEnglish
Published England Wiley Subscription Services, Inc 01.07.2022
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Abstract Pregnancy is a unique condition where the maternal immune system is continuously adapting in response to the stages of fetal development and signals from the environment. The placenta is a key mediator of the fetal/maternal interaction by providing signals that regulate the function of the maternal immune system as well as provides protective mechanisms to prevent the exposure of the fetus to dangerous signals. Bacterial and/or viral infection during pregnancy induce a unique immunological response by the placenta, and type I interferon is one of the crucial signaling pathways in the trophoblast cells. Basal expression of type I interferon‐β and downstream ISGs harbors physiological functions to maintain the homeostasis of pregnancy, more importantly, provides the placenta with the adequate awareness to respond to infections. The disruption of type I interferon signaling in the placenta will lead to pregnancy complications and can compromise fetal development. In this review, we focus the important role of placenta‐derived type I interferon and its downstream ISGs in the regulation of maternal immune homeostasis and protection against viral infection. These studies are helping us to better understand placental immunological functions and provide a new perspective for developing better approaches to protect mother and fetus during infections.
AbstractList Pregnancy is a unique condition where the maternal immune system is continuously adapting in response to the stages of fetal development and signals from the environment. The placenta is a key mediator of the fetal/maternal interaction by providing signals that regulate the function of the maternal immune system as well as provides protective mechanisms to prevent the exposure of the fetus to dangerous signals. Bacterial and/or viral infection during pregnancy induce a unique immunological response by the placenta, and type I interferon is one of the crucial signaling pathways in the trophoblast cells. Basal expression of type I interferon‐β and downstream ISGs harbors physiological functions to maintain the homeostasis of pregnancy, more importantly, provides the placenta with the adequate awareness to respond to infections. The disruption of type I interferon signaling in the placenta will lead to pregnancy complications and can compromise fetal development. In this review, we focus the important role of placenta‐derived type I interferon and its downstream ISGs in the regulation of maternal immune homeostasis and protection against viral infection. These studies are helping us to better understand placental immunological functions and provide a new perspective for developing better approaches to protect mother and fetus during infections.
Pregnancy is a unique condition where the maternal immune system is continuously adapting in response to the stages of fetal development and signals from the environment. The placenta is a key mediator of the fetal/maternal interaction by providing signals that regulate the function of the maternal immune system as well as provides protective mechanisms to prevent the exposure of the fetus to dangerous signals. Bacterial and/or viral infection during pregnancy induce a unique immunological response by the placenta, and type I interferon is one of the crucial signaling pathways in the trophoblast cells. Basal expression of type I interferon-β and downstream ISGs harbors physiological functions to maintain the homeostasis of pregnancy, more importantly, provides the placenta with the adequate awareness to respond to infections. The disruption of type I interferon signaling in the placenta will lead to pregnancy complications and can compromise fetal development. In this review, we focus the important role of placenta-derived type I interferon and its downstream ISGs in the regulation of maternal immune homeostasis and protection against viral infection. These studies are helping us to better understand placental immunological functions and provide a new perspective for developing better approaches to protect mother and fetus during infections.Pregnancy is a unique condition where the maternal immune system is continuously adapting in response to the stages of fetal development and signals from the environment. The placenta is a key mediator of the fetal/maternal interaction by providing signals that regulate the function of the maternal immune system as well as provides protective mechanisms to prevent the exposure of the fetus to dangerous signals. Bacterial and/or viral infection during pregnancy induce a unique immunological response by the placenta, and type I interferon is one of the crucial signaling pathways in the trophoblast cells. Basal expression of type I interferon-β and downstream ISGs harbors physiological functions to maintain the homeostasis of pregnancy, more importantly, provides the placenta with the adequate awareness to respond to infections. The disruption of type I interferon signaling in the placenta will lead to pregnancy complications and can compromise fetal development. In this review, we focus the important role of placenta-derived type I interferon and its downstream ISGs in the regulation of maternal immune homeostasis and protection against viral infection. These studies are helping us to better understand placental immunological functions and provide a new perspective for developing better approaches to protect mother and fetus during infections.
Author Hu, Anna
You, Yuan
Mor, Gil
Maxwell, Anthony
Ding, Jiahui
Liao, Aihua
Adzibolosu, Nicholas
AuthorAffiliation 1 C.S Mott center for Human Growth and Development, Department of Obstetrics and Gynecology, Wayne State University, Detroit, MI, USA
3 Institute of Reproductive Health, Center for Reproductive Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, PR China
2 Department of Physiology, Wayne State University, Detroit, MI, USA
AuthorAffiliation_xml – name: 1 C.S Mott center for Human Growth and Development, Department of Obstetrics and Gynecology, Wayne State University, Detroit, MI, USA
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Thu Apr 24 22:59:51 EDT 2025
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Issue 1
Keywords type I interferon
placenta
interferon-stimulated genes
ISG
trophoblast
pregnancy
Language English
License 2022 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.
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Notes This article is part of a series of reviews covering Immunity at the Maternal/Fetal interface appearing in Volume 308 of Immunological Reviews.
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content type line 14
ObjectType-Review-3
content type line 23
AUTHOR CONTRIBUTIONS
JD and GM wrote the document and prepared the figures. AM, NA, AH, YY and AL edited and discussed the document.
ORCID 0000-0002-5499-3912
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Snippet Pregnancy is a unique condition where the maternal immune system is continuously adapting in response to the stages of fetal development and signals from the...
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SubjectTerms Antiviral Agents
Developmental stages
Female
Fetus
Fetuses
Homeostasis
Humans
Immune response
Immune system
Immunity, Innate
Immunology
Immunoregulation
Interferon
Interferon Type I
interferon‐stimulated genes
ISG
Placenta
Pregnancy
Pregnancy complications
Signal Transduction
Signaling
trophoblast
type I interferon
Viral infections
Title Mechanisms of immune regulation by the placenta: Role of type I interferon and interferon‐stimulated genes signaling during pregnancy
URI https://onlinelibrary.wiley.com/doi/abs/10.1111%2Fimr.13077
https://www.ncbi.nlm.nih.gov/pubmed/35306673
https://www.proquest.com/docview/2675278310
https://www.proquest.com/docview/2641521460
https://pubmed.ncbi.nlm.nih.gov/PMC9189063
Volume 308
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