← BioTransfer GEO Dataset Finder
GEO series

Cell therapy with human IL-10-producing ILC2s limits xenogeneic Graft-versus-Host Disease by inhibiting pathogenic T cell responses

GSE278747 Homo sapiens (human) Single-cell RNA-seq 2 samples Submitted 2024/11/12 Platform GPL24676
At a glance

Single-cell RNA-seq · human · 2 samples

What it is
Single-cell RNA-seqGene activity measured in thousands of individual cells, so cell types can be told apart. Read from the summary: GEO's own type field only says 'expression profiling by sequencing', so confirm it in the paper.
Organism
Homo sapiens (human)
Samples
2 samples
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)
IL-10-producing group 2 innate lymphoid cells (ILC210) have important functions in regulating immune responses, yet their therapeutic potential remains largely unexplored. Here, we demonstrate that cell therapy with human ILC210 inhibits pathogenic T cell responses in humanized mouse models of Graft-versus-Host Disease (GVHD). Both prophylactic or post-onset adoptive transfer of human ILC210 significantly reduced GVHD severity and improved survival in NOD-scid IL2Rγnull (NSG) mice.
Read the full summary ↓
Notably, ILC210 provided comparable protection to regulatory T cells (Tregs) without impairing T cell engraftment, instead decreasing intestinal T cell infiltration and suppressing CD4+Th1 and CD8+Tc1. Additionally, ILC210 conferred superior protection from GVHD than conventional IL-10-/lowILC2s, and blocking IL-10 and IL-4 abrogated the protective effects of ILC210 cell therapy. In GVHD-protected HSCT recipients, ILC2s with an ILC210 phenotype were present at normal levels and inversely correlated with Th1 cells, consistent with findings in humanized mouse models. Critically, ILC210 did not impair T cell-mediated graft-versus-leukemia effects in a humanized model. CITE-seq analysis identified CD49d and CD86 as novel markers that allow for enrichment of ILC210 from conventional ILC2s, and to track ILC210 in patient studies. These results establish a platform for >2000-fold expansion of human ILC210 with a stable phenotype and underscore ILC210 potential in cell therapies for GVHD and other immune-mediated diseases.
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 GSE278747_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: Single-cell studies usually ship their counts as 10x files (matrix.mtx, barcodes.tsv, features.tsv), an .h5 file, or an .rds / .h5ad object that Seurat or Scanpy can open. Look for those among the supplementary files.

Also filed as BioProject PRJNA1168559. Searching any of these in the dataset finder brings you back here.

Samples in this study

The sample list for this study is not cached yet. Press Load samples and it will be fetched from NCBI.

+ 2 more — browse all 2 samples with per-sample file links →

Datasets on a similar topic

Search all human RNA-seq datasets in GEO →

Share this dataset

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.