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The CD49b (ITGA2) Collagen Receptor Excludes CD8+ T Cell Infiltration in Pancreatic Ductal Adenocarcinoma (PDAC)

GSE331086 Mus musculus (mouse) RNA-seq (gene expression) 9 samples Submitted 2026/06/01 Platform GPL21103
At a glance

RNA-seq (gene expression) · mouse · 9 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
9 samples: 3 × KPCWT pancreatic tumor, in vivo, vs 2 × KPCWT pancreatic cancer cell line, in vitro, vs 2 × KPC49bKO pancreatic cancer cell line, in vitro, vs 2 × KPC49bKO pancreatic tumor, in vivo,Groups 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)
PDAC is characterized by a dense desmoplastic stroma, contributing to tumor progression and immune evasion. This study investigates the functional role of CD49b in modulating anti-tumor immune responses and collagen architecture in PDAC. CD49b demonstrated a high tumor-specific expression compared to normal pancreatic tissues and peripheral blood mononuclear cells.
Read the full summary ↓
Loss of CD49b impaired PDAC cell adhesion to collagen, suppressed and delayed the tumor growth, and enhanced CD8+ T cell infiltration. In vivo depletion of CD8 T cells rescued the tumor growth in CD49b knock-out tumors. CD49b-knockout tumors showed increased secretion of CXCL10 chemokine, which drives T cell chemotaxis, while FAK signaling was downregulated. FAK overexpression restored tumor growth. CD49b knockout changed alignment of collagen fibers which was associated with a microenvironment permissive to immune infiltration. Targeting of CD49b with Vatelizumab disrupted PDAC cell adhesion and reduced tumor progression while increasing CD8+ T cells infiltration. CD49b is a key regulator of collagen-mediated immune interactions in PDAC, and these results support its potential as a therapeutic target.
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 GSE331086_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 PRJNA1466881 and SRA study SRP700926. Searching any of these in the dataset finder brings you back here.

Study design
3 × KPCWT pancreatic tumor, in vivo, vs 2 × KPCWT pancreatic cancer cell line, in vitro, vs 2 × KPC49bKO pancreatic cancer cell line, in vitro, vs 2 × KPC49bKO pancreatic tumor, in vivo,

Supports a between-group comparison across 9 samples.

How we read this: 4 replicated groups read from 9 sample titles; they account for 9 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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