Abstract
The placenta, the first and largest organ to develop after conception, not only nurtures and promotes the development of the conceptus, but, it also functions as a barrier against invading pathogens. Early phases of pregnancy are associated with expansion of specific subsets of Natural Killer cells (dNK) and macrophages (dMφ) at the maternal uterine mucosa, the basal decidua. In concert with cells of fetal origin, dNK cells, and dMφ orchestrate all steps of placenta and fetus development, and provide the first line of defense to limit vertical transmission. However, some pathogens that infect the mother can overcome this protective barrier and jeopardize the fetus health. In this review, we will discuss how members of the classical TORCH family (Toxoplasma, Other, Rubella, Cytomegalovirus, and Herpes simplex virus) and some emerging viruses (Hepatitis E virus, Zika virus, and SARS-CoV2) can afford access to the placental fortress. We will also discuss how changes in the intrauterine environment as a consequence of maternal immune cell activation contribute to placental diseases and devastating pregnancy outcomes.
Highlights
Human pregnancy is associated with tremendous changes of the maternal uterine mucosa, called decidua, to promote the implantation, and the development of the blastocyst
Minor immune cell subsets include innate lymphoid cells (ILCs) [13] and mucosal-associated invariant T cells (MAIT) [14]. The interaction of these immune cells with decidual stroma and invading fetal trophoblast cells is crucial for the establishment of an environment rich in soluble mediators including hormones, growth factors cytokines, chemokines and lipids, which are necessary for the development of the placenta and of the fetus. Given their dominance and active contribution to protection against pathogens, this review will mainly discuss the key features of dNK cells and dMφ during healthy pregnancy as well as their functional adaptations during viral invasion, and how viral infections disrupt the maternal-fetal barrier resulting in congenital infections
Lessons from the TORCH pathogens and emerging viruses have demonstrated that the infection of the maternal-fetal interface during early pregnancy is often associated with placental diseases and is highly detrimental to fetal development
Summary
Human pregnancy is associated with tremendous changes of the maternal uterine mucosa (endometrium), called decidua, to promote the implantation, and the development of the blastocyst. Minor immune cell subsets include innate lymphoid cells (ILCs) [13] and mucosal-associated invariant T cells (MAIT) [14] The interaction of these immune cells with decidual stroma and invading fetal trophoblast cells is crucial for the establishment of an environment rich in soluble mediators including hormones, growth factors cytokines, chemokines and lipids, which are necessary for the development of the placenta and of the fetus. Given their dominance and active contribution to protection against pathogens, this review will mainly discuss the key features of dNK cells and dMφ during healthy pregnancy as well as their functional adaptations during viral invasion, and how viral infections disrupt the maternal-fetal barrier resulting in congenital infections
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