GEO series

Targeting Bruton tyrosine kinase with acalabrutinib attenuates murine sclerodermatous chronic graft versus host disease

GSE310029 Mus musculus (mouse) RNA-seq (gene expression) 16 samples Submitted 2026/07/01 Platform GPL24247

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: 16 samples, each with a distinct title — no replicated groupsGroups 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.
Paper: Targeting Bruton tyrosine kinase with acalabrutinib attenuates murine sclerodermatous chronic graft versus host diseaseFrontiers in immunology · 2026

Summary (written by the submitters)

Allogeneic hematopoietic stem cell transplantation (allo-HSCT) is considered the only curative option for certain malignant hematopoietic disorders, yet its benefits are limited by the developmentof graft-versus-host disease (GVHD). Chronic GVHD (cGVHD) is often characterized by chronic inflammation and fibrosis, propagated by alloreactive donor B- and T-cell involvement.

Read the full summary ↓

Bruton tyrosine kinase (BTK) is the downstream effector in the B-cell receptor signaling pathway and further has a crucial role in mast cell activation, both of which are critical in the pathogenesis of cGVHD. Selective inhibition of BTK may be beneficial in ameliorating cGVHD pathogenesis. In this study, we evaluated the efficiency of acalabrutinib, a highly selective Bruton tyrosine kinase inhibitor using a murine sclerodermatous cGVHD model. Recipient BALB/c mice received total body irradiation (800cGy), followed by infusion of bone marrow and splenocytes of either syngeneic (BALB/c) or allogeneic (B10.D2) mice and were subsequently treated with acalabrutinib or control from starting three weeks after HSCT until end of week 8. Mice were monitored for clinical signs of GVHD, survival, organ pathology of skin and other organs, and inflammatory mediator expression in serum and skin. Acalabrutinib treatment showed better survival, improved clinical cGVHD scores, and reduced skin pathology. Significant reductions in dermal thickness and skin fibrosis, and mast cell numbers in the acalabrutinib-treated group. In vitro, experiments on mast cell activation show increased pro-inflammatory chemokines CCL2, CCL3, and CCL4 were effectively inhibited by acalabrutinib in a dose-dependent manner. Chemokine analysis from serum samples revealed significant differences in CXCL10, CXCL13, and CCL22 levels compared to the allogeneic control group. Furthermore, the acalabrutinib treatment showed decreased B220+ cells and CD3 infiltration in the skin. RNA-seq analysis of skin identified genes associated with keratinization were downregulated with acalabrutinib treatment. Our results demonstrate that specific inhibition of BTK with acalabrutinib has a potentially beneficial role in ameliorating cGVHD and warrants further investigation in patients with cGVHD.

Published in

Targeting Bruton tyrosine kinase with acalabrutinib attenuates murine sclerodermatous chronic graft versus host disease

Raguraman V, Mysinger M, Verma M et al. · Frontiers in immunology 2026 · PMID 42367798 · doi:10.3389/fimmu.2026.1843217

This dataset

Open GSE310029 in finder → Find more mouse RNA-seq datasets →

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.

Series matrix ↓

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 GSE310029_RAW.tar (it can run to tens of gigabytes).

All supplementary files ↗ Whole study · RAW.tar ↓

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.

Raw reads on ENA ↗

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 PRJNA1365024 and SRA study SRP644917. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 42367798) ↗

Study design

16 samples, each with a distinct title — no replicated groups

Any grouping that defines a comparison lives in the sample characteristics, which GEO records separately from the titles.

How we read this: Read from 16 sample titles: 16 distinct titles with little repetition. 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

GSM9286813 AC1_S42_L003
GSM9286814 AC2_S41_L003
GSM9286815 AC3_S43_L003
GSM9286816 AC4_S44_L003
GSM9286817 AC5_S45_L003
GSM9286818 AC6_S46_L003
GSM9286819 AL1_S31_L001
GSM9286820 AL2_S32_L001
GSM9286821 AL3_S33_L001
GSM9286822 AT1_S34_L001
GSM9286823 AT2_S35_L001
GSM9286824 AT3_S36_L001
GSM9286825 SC1_S27_L001
GSM9286826 SC2_S28_L001
GSM9286827 ST1_S29_L001
GSM9286828 ST2_S30_L001

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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.