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Regulatory T cells promote decidual vascular remodeling by modulating uterine natural killer cells to support pregnancy in mice

GSE267364 Mus musculus (mouse) RNA-seq (gene expression) 16 samples Submitted 2024/12/11 Platform GPL34328
At a glance

RNA-seq (gene expression) · mouse · 16 samples

What it is
RNA-seq (gene expression)Gene activity measured by sequencing. The summary does not mention single-cell work, so this is most likely bulk: one average per sample, the usual starting point for comparing groups.
Organism
Mus musculus (mouse)
Samples
16 samples: 6 × Decidua, vehicle treated vs 5 × Decidua, DT treated vs 5 × Decidua, DT+Treg treatedGroups are read from the sample names, not from the paper. Check the list below.
Data you can get
A processed table (series matrix) and supplementary files from NCBI; the raw sequencing reads from ENA. Which of these hold counts depends on the study, so check the file list.
Summary (written by the submitters)
Regulatory T (Treg) cells are essential for maternal immune tolerance of the fetus and placenta. In preeclampsia, aberrant Treg cell tolerance is implicated, but whether and how Treg cells affect the uterine vascular dysfunction thought to precede placental impairment and maternal vasculopathy is unclear. We utilized Foxp3 DTR mice to test the hypothesis that Treg cells are essential regulators of decidual spiral artery adaptation to pregnancy.
Read the full summary ↓
Transient Treg cell depletion during early placental morphogenesis caused impaired remodeling of decidual spiral arteries and altered uterine artery function, resulting in late gestation fetal loss and fetal growth restriction. Treg cell depletion impaired acquisition of the activation receptor NKp46 on uterine natural killer (uNK cells) and was associated with reduced decidual synthesis of Treg cell-derived cytokines Il35, Il10 and Tgfb implicated in modulating uNK cell phenotype. When Treg cells were replaced, the adverse impact on uNK cell abundance and phenotype, decidual spiral artery remodeling, uterine artery function, and fetal loss was mitigated. These data implicate Treg cells as essential upstream drivers of uterine vascular adaptation to pregnancy through regulation of uNK cell recruitment and activation. The findings provide a mechanism linking impaired adaptive immune tolerance and altered spiral artery remodeling, two hallmark features of preeclampsia.
This dataset
Download · which file do I need?

Direct links to NCBI and ENA, no account and no request form. Pick by what you want to do: take the small processed table to look, the supplementary files to re-analyse, or the original raw data to start over.

1 · Just have a look

Processed table

The series matrix: one table of values per sample as the submitters processed it. The smallest download, and it opens in Excel or R. Start here to see what the data look like.

2 · Re-analyse it

Supplementary files

The count tables and other files the authors uploaded. Take only the samples you need, or the whole study as GSE267364_RAW.tar (it can run to tens of gigabytes).

3 · Start from the raw reads

Raw sequencing reads

The original FASTQ files, straight from the sequencer, held at ENA. Large, and you align them yourself, so only choose this if you need to re-process the study from scratch.

What the files usually look like: For RNA-seq the counts are usually a table among the supplementary files (look for 'counts', 'expression', 'FPKM' or 'TPM' in the file name). The series matrix of a sequencing study is sometimes nearly empty.

Also filed as BioProject PRJNA1111144 and SRA study SRP507418. Searching any of these in the dataset finder brings you back here.

Study design
6 × Decidua, vehicle treated vs 5 × Decidua, DT treated vs 5 × Decidua, DT+Treg treated

Supports a between-group comparison across 16 samples.

How we read this: 3 replicated groups read from 16 sample titles; they account for 16 of them. These groups are guessed from the sample names, not taken from the paper, so check them against the sample list below before relying on them.

Samples in this study
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Metadata from NCBI GEO, cached and refreshed periodically — the NCBI page above is authoritative. Downloads link straight to NCBI/ENA; nothing is proxied through BioTransfer.