Abstract
Decidual natural killer (dNK) cells are the tissue-resident and major subpopulation of NK cells at the maternal-fetal interface. It has been demonstrated that dNK cells play pivotal roles in pregnancy, including keeping maternal-fetal immune tolerance, promoting extravillous trophoblast (EVT) cell invasion, and driving uterine spiral artery remodeling. However, the molecular mechanisms haven’t been elucidated until recent years. In this review, we systemically introduce the generation, subsets, and surface or soluble molecules of dNK cells, which are critical for maintaining the functions of dNK cells. Further, new functions of dNK cells including well-controlled cytotoxicity, immunosurveillance and immunotrophism supporting via the cell-cell interaction between dNK cells and EVT cells are mainly focused. The molecular mechanisms involved in these functions are also illustrated. Moreover, pregnancy-associated diseases caused by the dNK cells abnormalities are discussed. It will be important for future investigations about the mechanism of maintenance of pregnancy and parturition and potential clinical applications of dNK cells.
Highlights
The maternal-fetal interface, between the endometrium and extraembryonic tissue, plays pivotal roles in nutrient transportation, gas exchange, immune tolerance and protection for maintenance of pregnancy
It may have three origins of Decidual natural killer (dNK) cells: 1 CD16- NK cells are attracted by chemokines and immigrate from peripheral blood into decidua directly, where they differentiate into dNK cells under decidual microenvironment. 2 dNK cells are differentiated from hematopoietic progenitor cells in the uterus. 3 dNK cells are directly converted from the CD16+ peripheral NK (pNK) cells
In addition to the surface molecules, there are many soluble molecules secreted by dNK cell subsets, such as chemokines, granulocyte-macrophage colony-stimulating factor (GM-CSF), interferon g (IFN-g), vascular endothelial-derived growth factor (VEGF), angiopoietin (Ang), placental growth factor (PLGF), soluble Fas ligand, matrix metalloproteinase (MMP-2), MMP-9 and transforming growth factor-beta (TGF-b) [17, 49, 50]
Summary
The maternal-fetal interface, between the endometrium and extraembryonic tissue, plays pivotal roles in nutrient transportation, gas exchange, immune tolerance and protection for maintenance of pregnancy. The dynamic process of formation of the functional maternal-fetal interface mainly includes extravillous trophoblast (EVT) cell invasion, spiral arteriole remodeling, and establishment of the tolerant immune microenvironment [1,2,3]. Rather than immunosurveillance, dNK cells are modified and mainly responsible for immune tolerance to the fetus, EVT cell invasion, and uterine spiral artery remodeling by interacting with EVT cells at the maternal-fetal interface [2]. The molecular mechanisms have attracted much attention They haven’t been fully elucidated for the dynamic complexity of multi-cell interactions. The elucidated molecular mechanisms would help us understand pregnancy progress and provide new strategies for precision treatment of pregnancy-related diseases
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