The central role of natural killer cells in preeclampsia

Preeclampsia (PE) is a disease that is unique to pregnancy and affects multiple systems. It can lead to maternal and perinatal mortality. The precise etiology of PE is unclear. Patients with PE may have systemic or local immune abnormalities. A group of researchers has proposed that the immune commu...

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Bibliographic Details
Published inFrontiers in immunology Vol. 14; p. 1009867
Main Authors Wei, Xiaoqi, Yang, Xiuhua
Format Journal Article
LanguageEnglish
Published Switzerland Frontiers Media S.A 14.02.2023
Subjects
Arteries
Communication
Female
HLA-C Antigens
Humans
immune
Immunology
Killer Cells, Natural
NK cells
placenta
Pre-Eclampsia
preeclampsia
Pregnancy
placenta
NK cells
immune
preeclampsia
pregnancy
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Summary:Preeclampsia (PE) is a disease that is unique to pregnancy and affects multiple systems. It can lead to maternal and perinatal mortality. The precise etiology of PE is unclear. Patients with PE may have systemic or local immune abnormalities. A group of researchers has proposed that the immune communication between the fetus and mother is primarily moderated by natural killer (NK) cells as opposed to T cells, since NK cells are the most abundant immune cells in the uterus. This review examines the immunological roles of NK cells in the pathogenesis of PE. Our aim is to provide obstetricians with a comprehensive and updated research progress report on NK cells in PE patients. It has been reported that decidual NK (dNK) cells contribute to the process of uterine spiral artery remodeling and can modulate trophoblast invasion. Additionally, dNK cells can stimulate fetal growth and regulate delivery. It appears that the count or proportion of circulating NK cells is elevated in patients with or at risk for PE. Changes in the number or function of dNK cells may be the cause of PE. The Th1/Th2 equilibrium in PE has gradually shifted to an NK1/NK2 equilibrium based on cytokine production. An improper combination of killer cell immunoglobulin-like receptor (KIR) and human leukocyte antigen (HLA)-C may lead to insufficient activation of dNK cells, thereby causing PE. In the etiology of PE, NK cells appear to exert a central effect in both peripheral blood and the maternal-fetal interface. To maintain immune equilibrium both locally and systemically, it is necessary to take therapeutic measures directed at NK cells.
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This article was submitted to NK and Innate Lymphoid Cell Biology, a section of the journal Frontiers in Immunology
Edited by: Cristina Bottino, University of Genoa, Italy
Reviewed by: Silvia Pesce, University of Genoa, Italy; Sonja Suvakov, Mayo Clinic, United States
ISSN:1664-3224
1664-3224
DOI:10.3389/fimmu.2023.1009867