Several cytokines including EGF, GM-CSF, IFN. channels superimposed (right). White arrows point to labeled cells. Bars represent 50m.(PDF) pone.0164353.s002.pdf (6.4M) GUID:?A1F4319C-110E-423A-8CCC-15BF684F6A70 S1 File: Cell type pair-wise comparisons. List of genes differentially expressed with at least a two fold change and false discovery rate (FDR) of 0.05 in different pair-wise cell type comparisons.(XLSX) pone.0164353.s003.xlsx (3.4M) GUID:?12989AD5-625A-4177-9D40-D90E7465054E Exemestane S2 File: Comparison of gene expression changes between dNK and idNK cells from pNK cells. First tabTranscripts differentially expressed with at least a 2 fold change and a FDR 5% between dNK and CD56Bright pNK cells (first tab). Graph shows change in gene expression in CD56Bright pNK vs. dNK in blue bars, and CD56Bright pNK vs. CD56Bright idNK (shown in red bars if fold change was greater than 2 and FDR 5%, or green bars if they did not meet these two criteria). Second Tab- Transcripts differentially expressed with at least a 2 fold change and a FDR 5% between dNK and CD56Dim pNK cells). Graph shows change in gene expression in CD56dim pNK vs. dNK in blue bars, and CD56Dim pNK vs. CD56Dim idNK (shown in red bars if fold change was greater than 2 and FDR 5%, or green bars if they did not meet these two criteria).(XLSX) pone.0164353.s004.xlsx (360K) GUID:?FFEF711E-7450-445F-9459-978E5C0085D2 S3 File: Pathway enrichment analysis. 136 pathways significantly affected (P value 0.001) in at least one of the following pair wise comparisons: idNK_CD56Dim vs. dNK, idNK_CD56Bright vs. dNK, pNK_CD56Bright Exemestane vs. dNK, pNK_CD56Dim vs. dNK or pNK_CD56Bright vs. pNK_CD56Dim. The P value is usually a significance level with smaller P values indicating increasing confidence in the effect around the pathway.(XLSX) pone.0164353.s005.xlsx (21K) GUID:?9DF9E6E5-1494-49A5-9B7D-39958C1821B7 S1 Table: Complete cytokine secretion data of idNK cells. Supernatants from idNK Exemestane and control pNK IL-15 collected at 7 days were measured for a panel of 46 cytokines, angiogenic factors and growth factors from two overlapping luminex kits. P-values shown are derived from two-tailed t-tests comparing the mean concentration of each analyte in supernatants of idNK cells vs. pNK cells from three donors. ** p 0.01, *p 0.05. pNK cells 24hs baseline expression correspond to new pNK cell from three impartial donors cultured 24hs in the presence of IL15.(PDF) pone.0164353.s006.pdf (72K) GUID:?83A598C4-777A-44C9-B4BF-471D0E6F4444 S2 Table: pNK to idNK conversion efficiency of cell preparations injected in mice. idNK conversion efficiency was evaluated by the percentage of CD9+KIR+cells in CD3-CD56BrightCD16- NK cell and in CD3-CD56DimCD16+ cell populations in the culture. Mice were injected with cells from the donor indicated in the table.(PDF) pone.0164353.s007.pdf (161K) GUID:?3345F662-62BC-4DC0-A937-E386DF1C1D54 Data Availability StatementRaw microarray data was deposited in NCBI GEO Database (GSE85592). Abstract Decidual NK (dNK) cells, a distinct type of NK cell, are thought to regulate uterine spiral artery remodeling, a process that allows for increased blood delivery to the fetal-placental unit. Impairment of uterine spiral artery remodeling is associated with decreased placental perfusion, increased uterine artery resistance, and obstetric complications such as preeclampsia and intrauterine growth restriction. manipulation of human peripheral blood NK (pNK) cells by a combination of hypoxia, TGF?-1 and 5-aza-2-deoxycytidine yields Exemestane cells with phenotypic and functional similarities to dNK Rabbit Polyclonal to IkappaB-alpha cells, called idNK cells. Here, gene expression profiling shows that CD56Bright idNK cells derived from human pNK cells, and to a lesser extent CD56Dim idNK cells, are enriched in the gene expression signature that distinguishes dNK cells from pNK cells. When injected into immunocompromised pregnant mice with elevated uterine artery resistance, idNK cells homed to the Exemestane uterus and reduced the uterine artery resistance index, suggesting improved placental perfusion. Introduction Abnormal placentation sets the stage for the development of pregnancy complications that may present with devastating maternal and fetal outcomes. The mechanisms that regulate placental development remain elusive. Natural killer (NK) cells at the maternal-fetal interface are increasingly recognized as important players in this process[1,2]. Human NK cells are lymphocytes characterized by high cytolytic potential against tumor-transformed and virus-infected cells. Peripheral blood NK cells (pNK) represent.