Placental regulation of immune functions

Smith, Arianna; Aldo, Paulomi; Racicot, Karen

doi:10.1016/b978-0-12-818508-7.00004-x

Cited by 2 publications

(2 citation statements)

References 77 publications

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“…30 In addition, macrophages are another important cellular component modulating the inflammatory milieu at the implantation site. 32 During early implantation, macrophages present at the decidua are M1 type 33,34 and produce inflammatory cytokines such as TNFα 35 ; necessary for the modulation of cytokines and chemokines produced by the stroma. 36 Consequently, the modification of the type of macrophages present in the second phase of the implantation process is critical for the inflammatory shift.…”

Section: Immune Homeos Ta S Is Of Preg Nan C Ymentioning

confidence: 99%

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

Ding

Maxwell

Adzibolosu

et al. 2022

Immunological Reviews

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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.

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Section: Immune Homeos Ta S Is Of Preg Nan C Ymentioning

confidence: 99%

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

Ding

Maxwell

Adzibolosu

et al. 2022

Immunological Reviews

View full text Add to dashboard Cite

show abstract

“…It is also associated with longterm adverse health outcomes in offspring, to include asthma, and other immune disorders, and neurocognitive and metabolic disorders [4]. Notably, the incidence of these health outcomes is often dominant in one sex over another [5][6][7][8][9][10][11]. Using a mouse model of low-grade prenatal stress during late pregnancy, we previously showed that mice born to dams with elevated stress hormone have heightened responses to airway allergen when compared to controls, and that these responses differ based on sex of the offspring [9].…”

Section: Introductionmentioning

confidence: 99%

Exogenous corticosterone administration during pregnancy alters placental and fetal thyroid hormone availability in females

Paul,

Shubitidze,

Rahim

et al. 2023

Preprint

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Introduction: Maternal prenatal stress is associated with adverse pregnancy outcomes and predisposition to long-term adverse health outcomes in children. While the molecular mechanisms that govern these associations have not been fully teased apart, stress-induced changes in placental function can drive sex-specific phenotypes in offspring. We sought to identify and examine molecular pathways in the placenta that are altered in response to maternal prenatal stress. Methods: Using a mouse model of maternal prenatal stress, we conducted RNA-seq analysis of whole placenta at E18.5. We used qRT-PCR to validate gene expression changes in the placenta and in a trophoblast cell line. ELISAs were used to measure the abundance of thyroid hormones in maternal and fetal serum and in the placenta. Results: Dio2 was amongst the top differentially expressed genes in response to elevated maternal stress hormone. Dio2 expression was more downregulated in female placenta from stressed dams than both female control and male placenta. Consistent with Dio2's role in production of bioactive thyroid hormone (T3), we found that there was a reduction of T3 in placenta and serum of female embryos from stressed dams at E18.5. Both T3 and T4 were reduced in the fetal compartment of the female placenta from stressed dams at E16.5. Stress hormone induced reduction in thyroid hormone in females was independent of circulating levels of TH in the dams. Discussion: The placental thyroid hormone synthesis pathway may be a target of maternal stress and modulate fetal programming of health and disease of offspring in a sex-specific fashion.

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Placental regulation of immune functions

Cited by 2 publications

References 77 publications

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

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

Exogenous corticosterone administration during pregnancy alters placental and fetal thyroid hormone availability in females

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