← BioTransfer GEO Dataset Finder
GEO series

Molecular mechanisms underlying the modulation of T-cell proliferation and cytotoxicity by immobilized CCL21 and ICAM1

GSE254335 Mus musculus (mouse) RNA-seq (gene expression) 52 samples Submitted 2024/06/28 Platform GPL24247
At a glance

RNA-seq (gene expression) · mouse · 52 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
52 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.
Paper
Molecular mechanisms underlying the modulation of T-cell proliferation and cytotoxicity by immobilized CCL21 and ICAM1Journal for immunotherapy of cancer · 2024
Summary (written by the submitters)
A major challenge in adoptive cancer immunotherapy is the effective balance between the proliferation and cytotoxic capacity of the effector CD8+ T-cells. In this study we explored the molecular mechanisms whereby a “synthetic immune niche” (SIN), composed of immobilized CCL21 and ICAM1, modulates the interplay between these two cellular properties.
Read the full summary ↓
Temporal phenotypic profiling of OVA-specific murine T-cells revealed major differences in the response to the SIN stimulation following antigen-specific and non-specific activation. Thus, SIN treatment enhanced both the expansion and cytotoxicity of cells activated by OVA-loaded DCs, at day 4, while, similar treatment of cells activated by anti CD3/CD28-conjugated beads dramatically enhanced the cells’ expansion, but unexpectedly blocked their cytotoxicity, which fully recovered only on day 7. Molecular profiling suggest that upregulation of cytotoxic gene signatures drive the SIN effect following DC activation, while down-regulation of exhaustion and pro-apoptotic genes optimize the proliferation-cytotoxicity balance in the beads-activated cells.
Published in
Molecular mechanisms underlying the modulation of T-cell proliferation and cytotoxicity by immobilized CCL21 and ICAM1
Yado S, Dassa B, Zoabi R et al. · Journal for immunotherapy of cancer 2024 · PMID 38866588 · doi:10.1136/jitc-2024-009011
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 GSE254335_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 PRJNA1069759 and SRA study SRP486163. 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.

+ 52 more — browse all 52 samples with per-sample file links →

Datasets on a similar topic

Search all mouse 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.