Decidualization and angiogenesis in early pregnancy: unravelling the functions of DC and NK cells

The actors of human implantation: gametes, embryo and endometrium

“…Finally, hCG treatment of activated dendritic cells results in an upregulation of MHC class II, IL-10 and IDO expression, reducing the ability to stimulate T cell proliferation. Impact of dendritic cells during implantation has recently been review by Blois (Blois et al, 2011).…”

“…Failure to express adequate decidualization pattern is likely to induce early pregnancy lost or predispose to obstetrical complications such as implantation failure, recurrent miscarriages, pre-eclampsia, fetal growth restriction... (Blois et al, 2011;Brosens, 2011;Plaisier, 2011).…”

“…These cells secrete an array of cytokines important for adequate local immune regulation, angiogenesis, placental development, and establishment of pregnancy. Other immune cells or systems such as dendritic cells, T regulatory cells, macrophages, Th1/Th2 equilibrium orchestrate immune tolerance, trophoblast invasion and angiogenesis associated with embryo implantation (Blois et al, 2011;Denney et al, 2011).…”

Estrogen Receptors in Leukocytes - Possible Impact on Inflammatory Processes in the Female Reproductive System

“…Leukocytes are present in large amounts during decidualization indicating their participation in the process (Guo et al, 2011). Studies in mice showed that uNK cells promote uterine vascular cell remodeling that assist decidual growth (Blois et al, 2011). Certain uNK cell derived chemokines and cytokines can influence the gene expression profile of human endometrial fibroblasts in vitro suggesting that a similar mechanism could operate in the endometrium (Germeyer et al, 2009).…”

“…uNK cells express ER and it may exert control over trophoblast invasion (Henderson et al, 2003;Kwak-Kim & Gilman-Sachs, 2008). They also promote uterine vascular modifications assisting decidual growth during early pregnancy (Blois et al, 2011). Regulation of inflammation during implantation may follow a sequential model in which pro-inflammation is followed by anti-inflammation or there may be a continuous balance between the pro-and anti-inflammatory environments (Jabbour et al, 2009).…”