Abstract
Recurrent pregnancy loss (RPL), especially the unexplained RPL, is associated with the disruption of maternal immune tolerance. However, little is known about the immune status at the decidua of RPL with embryonic chromosomal aberrations. Herein, mass cytometry (CyTOF) was used to interrogate the immune atlas at the decidua which was obtained from 15 RPL women—six with normal chromosome and nine with chromosomal aberrations—and five controls. The total frequency of CCR2−CD11chigh macrophages increased, while CD39high NK cells and CCR2−CD11clow macrophages decrease significantly in RPL when RPLs were stratified, compared with controls. Pro-inflammatory subsets of CD11chigh macrophages increased, while less pro-inflammatory or suppressive subsets decreased statistically in RPL decidua whenever RPLs were stratified or not. However, CD11chigh NK and CD161highCD8+ T cells increased only in RPL with normal chromosome, while the inactivated and naive CD8+/CD4+ T cells were enriched only in RPL with chromosomal aberrations. A pro-inflammatory signature is observed in RPL decidua; however, differences exist between RPL with and without chromosomal abnormalities.
Highlights
Recurrent pregnancy loss (RPL) is defined as two or more consecutive pregnancy losses before the 20th week of gestation and occurs in about 1%–3% of reproductive women [1]
Decidual NK cells possess a CD56brightCD16− phenotype and account for 50%–70% of leukocytes in the first trimester. They modulate trophoblast invasion by producing IL-8 and IL-10 and initiate artery remodeling through secreting vascular endothelial growth factor (VEGF) and arginase-1 [5, 6]. dNK plays an important role in extravillous trophoblast (EVT) cells acquiring invasive phenotype and invasive EVT gaining endothelial-like properties [8]
The percentages of M2 macrophages statistically decreased in both RPL subgroups when they were stratified, compared with controls (Figure 1D), while variation existed among the individuals (Figures 1E, F)
Summary
Recurrent pregnancy loss (RPL) is defined as two or more consecutive pregnancy losses before the 20th week of gestation and occurs in about 1%–3% of reproductive women [1]. With the number of miscarriages increased, the recurrent risk of pregnancy loss raises quickly from about 11% at one loss to 40% after three or more losses [2]. Though possible causes including uterine malformations, maternal infection, endocrine disorders, and genetic abnormalities have been identified, only maternal age and the number of prior pregnancy losses are considered as prognostic factors for. Decidual NK cells (dNKs) possess a CD56brightCD16− phenotype and account for 50%–70% of leukocytes in the first trimester. They modulate trophoblast invasion by producing IL-8 and IL-10 and initiate artery remodeling through secreting vascular endothelial growth factor (VEGF) and arginase-1 [5, 6]. Decidual non-NK ILCs are mainly ILC3 and participate in tissue remodeling by expressing IL-22 and IL-8 or inducing decidual stromal cell (DSC) to express adhesion molecules [9]
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