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JAK/STAT inhibition restores disease tolerance in malaria-infected glucocorticoid receptor knockout mice.

GSE268268 Mus musculus (mouse) RNA-seq (gene expression) 18 samples Submitted 2025/06/19 Platform GPL21103
At a glance

RNA-seq (gene expression) · mouse · 18 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
18 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
JAK/STAT inhibition protects glucocorticoid receptor knockout mice from lethal malaria-induced hypoglycemia and hyperinflammationEMBO molecular medicine · 2025
Summary (written by the submitters)
Disease tolerance is a defense strategy, whereby the host limits tissue damage, without affecting the pathogen load. In malaria, the disease tolerance mechanisms by which many infected individuals are protected against severe disease, are still incompletely understood. In this study, we show that endogenous glucocorticoids are integral components of disease tolerance in malaria, as genetic deletion of the glucocorticoid receptor in mice resulted in the development of lethal hypoglycemia during Plasmodium chabaudi AS infection.
Read the full summary ↓
This was paralleled by altered metabolism in liver and spleen, marked by increased glucose uptake, a predominant glycolytic transcriptome, reduced gluconeogenic gene expression and depletion of glycogen stores. Hypoglycemia was highly associated with activation of the JAK/STAT pathway in the liver and spleen. Treatment with ruxolitinib, a JAK1/2 inhibitor, ensured survival by protecting against lethal hypoglycemia. These findings highlight the pivotal role of endogenous glucocorticoids in disease tolerance, and suggest a potential therapeutic role for ruxolitinib in managing malaria-induced hypoglycemia.
Published in
JAK/STAT inhibition protects glucocorticoid receptor knockout mice from lethal malaria-induced hypoglycemia and hyperinflammation
Prenen F, Vandermosten L, Knoops S et al. · EMBO molecular medicine 2025 · PMID 40702267 · doi:10.1038/s44321-025-00264-w
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 GSE268268_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 PRJNA1116062 and SRA study SRP509715. Searching any of these in the dataset finder brings you back here.

Samples in this study

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