scholarly journals Dynamic Function and Composition Changes of Immune Cells During Normal and Pathological Pregnancy at the Maternal-Fetal Interface

2019 ◽  
Vol 10 ◽  
Author(s):  
Fenglian Yang ◽  
Qingliang Zheng ◽  
Liping Jin
2020 ◽  
Vol 218 (1) ◽  
Author(s):  
Christina Megli ◽  
Carolyn B. Coyne

In this issue of JEM, Thomas et al. (https://doi.org/10.1084/jem.20200891) provide elegant technological and conceptual advances that further our understanding of the immune cells enriched at the maternal–fetal interface. Using new isolation strategies to better separate maternal- and fetal-derived cells, the authors identify previously undefined maternal-derived immune cells associated with the fetal-derived placenta and provide an in-depth analysis of the markers and characteristics of placental Hofbauer cells.


2020 ◽  
Author(s):  
Petoria Gayle ◽  
Vanessa McGaughey ◽  
Rosmely Hernandez ◽  
Marina Wylie ◽  
Rachel C. Colletti ◽  
...  

AbstractPlacental immune responses are highly regulated to strike a balance between protection and tolerance. For relatively mild infections, protection encompasses both the mother and fetus; however, during worsening conditions, protection becomes exclusively reserved for the mother. Previously, we and others have shown that the host factor Perforin-2 plays a central role in protecting mice and cells against infection. Here, we analyzed Perforin-2 activity in the mouse placenta to determine whether Perforin-2 plays a similarly protective role. We show that Perforin-2 is critical for inhibiting Listeria monocytogenes colonization of the placenta and fetus and that this protection is due to both maternal and fetal-encoded Perforin-2. Perforin-2 mRNA is readily detectable in individual immune cells of the decidua and these levels are further enhanced specifically in decidual macrophages during high-dose infections that result in fetal expulsion. Unexpectedly, inductive Perforin-2 expression in decidual macrophages did not occur during milder infections in which fetal viability remained intact. This pattern of expression significantly differed from that observed in splenic macrophages in which inductive Perforin-2 expression was observed in both high and mild infection conditions. In the placenta, inductive Perforin-2 expression in decidual macrophages was co-incident with their polarization from a M2 to M1 phenotype that normally occurs in the placenta during high-burden infections. Our results suggest that Perforin-2 is part of a host response that is protective either for both the mother and fetus in milder infections or exclusively for the mother during high-dose infections.


2019 ◽  
Vol 198 (1) ◽  
pp. 15-23 ◽  
Author(s):  
E. Giacomini ◽  
E. Alleva ◽  
G. Fornelli ◽  
A. Quartucci ◽  
L. Privitera ◽  
...  

Author(s):  
Jennet Baltayeva ◽  
Chaini Konwar ◽  
Barbara Castellana ◽  
Danielle L Mara ◽  
Julian K Christians ◽  
...  

Abstract Prepregnancy obesity associates with adverse reproductive outcomes that impact maternal and fetal health. While obesity-driven mechanisms underlying adverse pregnancy outcomes remain unclear, local uterine immune cells are strong but poorly studied candidates. Uterine immune cells, particularly uterine natural killer cells (uNKs), play central roles in orchestrating developmental events in pregnancy. However, the effect of obesity on uNK biology is poorly understood. Using an obesogenic high-fat/high-sugar diet (HFD) mouse model, we set out to examine the effects of maternal obesity on uNK composition and establishment of the maternal–fetal interface. HFD exposure resulted in weight gain-dependent increases in systemic inflammation and rates of fetal resorption. While HFD did not affect total uNK frequencies, HFD exposure did lead to an increase in natural cytotoxicity receptor-1 expressing uNKs as well as overall uNK activity. Importantly, HFD-associated changes in uNK coincided with impairments in uterine artery remodeling in mid but not late pregnancy. Comparison of uNK mRNA transcripts from control and HFD mice identified HFD-directed changes in genes that play roles in promoting activity/cytotoxicity and vascular biology. Together, this work provides new insight into how obesity may impact uNK processes central to the establishment of the maternal–fetal interface in early and mid pregnancy. Moreover, these findings shed light on the cellular processes affected by maternal obesity that may relate to overall pregnancy health.


2016 ◽  
Vol 118 ◽  
pp. 92-99 ◽  
Author(s):  
Xiao-Hui Hu ◽  
Mao-Xing Tang ◽  
Gil Mor ◽  
Ai-Hua Liao

2019 ◽  
Vol 20 (15) ◽  
pp. 3654 ◽  
Author(s):  
Andrea Olmos-Ortiz ◽  
Pilar Flores-Espinosa ◽  
Ismael Mancilla-Herrera ◽  
Rodrigo Vega-Sánchez ◽  
Lorenza Díaz ◽  
...  

During pregnancy, the placenta, the mother and the fetus exploit several mechanisms in order to avoid fetal rejection and to maintain an immunotolerant environment throughout nine months. During this time, immune cells from the fetal and maternal compartments interact to provide an adequate defense in case of an infection and to promote a tolerogenic milieu for the fetus to develop peacefully. Trophoblasts and decidual cells, together with resident natural killer cells, dendritic cells, Hofbauer cells and other macrophages, among other cell types, contribute to the modulation of the uterine environment to sustain a successful pregnancy. In this review, the authors outlined some of the various roles that the innate immune system plays at the maternal–fetal interface. First, the cell populations that are recruited into gestational tissues and their immune mechanisms were examined. In the second part, the Toll–like receptor (TLR)–dependent immune responses at the maternal–fetal interface was summarized, in terms of their specific cytokine/chemokine/antimicrobial peptide expression profiles throughout pregnancy.


Reproduction ◽  
2010 ◽  
Vol 140 (6) ◽  
pp. 803-813 ◽  
Author(s):  
Judith E Cartwright ◽  
Rupsha Fraser ◽  
Karin Leslie ◽  
Alison E Wallace ◽  
Joanna L James

In human pregnancy, successful placentation and remodelling of the uterine vasculature require the integration of a number of stages, which are crucial for a healthy pregnancy. As the demands of the developing fetus for nutrients and oxygen increase, the capacity of the maternal blood vessels to supply this must be altered radically, with deficiencies in this process implicated in a number of dangerous pregnancy complications. The complex signalling networks that regulate these tightly co-ordinated events are becoming clearer as more studies of early pregnancy are performed. It is the aim of this review to draw together our knowledge of events that occur to facilitate a successful pregnancy ranging from the preparation for implantation, through the invasion and differentiation of the trophoblast and the regulation of these processes by other cells within the decidual environment, to the active role that the trophoblast and maternal immune cells play in facilitating the remodelling of the uterine spiral arteries. The events involved in a healthy pregnancy will then be compared to aberrant placentation and remodelling, which are characteristics of many pregnancy disorders, and recent advances in detection of abnormal placental development will also be discussed.


2015 ◽  
Vol 13 (4) ◽  
pp. 462-473 ◽  
Author(s):  
Marcia Arenas-Hernandez ◽  
Roberto Romero ◽  
Derek St Louis ◽  
Sonia S Hassan ◽  
Emily B Kaye ◽  
...  

2021 ◽  
Vol 5 (6) ◽  
pp. 20-23
Author(s):  
Jingyi Wang ◽  
Nan Li

This article is a summary of the research progress of the maternal-fetal interface immune microenvironment regulated by traditional Chinese medicine in the treatment of recurrent spontaneous abortion. The imbalance of the immune microenvironment at the maternal-fetal interface is closely related to the occurrence of recurrent spontaneous abortion. Traditional Chinese medicine can maintain the homeostasis of the immune microenvironment at the maternal-fetal interface by regulating the function of immune cells and the expression of related cytokines.


2019 ◽  
Vol 2019 ◽  
pp. 1-16 ◽  
Author(s):  
Rebecca Slutsky ◽  
Roberto Romero ◽  
Yi Xu ◽  
Jose Galaz ◽  
Derek Miller ◽  
...  

Successful pregnancy requires a tightly-regulated equilibrium of immune cell interactions at the maternal-fetal interface (i.e., the decidual tissues), which plays a central role in the inflammatory process of labor. Most of the innate immune cells in this compartment have been well characterized; however, adaptive immune cells are still under investigation. Herein, we performed immunophenotyping of the decidua basalis and decidua parietalis to determine whether exhausted and senescent T cells are present at the maternal-fetal interface and whether the presence of pathological (i.e., preterm) or physiological (i.e., term) labor and/or placental inflammation alter such adaptive immune cells. In addition, decidual exhausted T cells were sorted to test their functional status. We found that (1) exhausted and senescent T cells were present at the maternal-fetal interface and predominantly expressed an effector memory phenotype, (2) exhausted CD4+ T cells increased in the decidua parietalis as gestational age progressed, (3) exhausted CD4+ and CD8+ T cells decreased in the decidua basalis of women who underwent labor at term compared to those without labor, (4) exhausted CD4+ T cells declined with the presence of placental inflammation in the decidua basalis of women with preterm labor, (5) exhausted CD8+ T cells decreased with the presence of placental inflammation in the decidua basalis of women who underwent labor at term, (6) both senescent CD4+ and CD8+ T cells declined with the presence of placental inflammation in the decidua basalis of women who underwent preterm labor, and (7) decidual exhausted T cells produced IFNγ and TNFα upon in vitro stimulation. Collectively, these findings indicate that exhausted and senescent T cells are present at the human maternal-fetal interface and undergo alterations in a subset of women either with labor at term or preterm labor and placental inflammation. Importantly, decidual T cell function can be restored upon stimulation.


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