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Type-I interferon priming signal balances anti-bacterial and anti-tumor trained immunity in alveolar macrophages [RNA-seq]

GSE295483 Mus musculus (mouse) RNA-seq (gene expression) 19 samples Submitted 2025/05/07 Platform GPL24247
At a glance

RNA-seq (gene expression) · mouse · 19 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
19 samples: 3 × IFNAR-/-PBS AMs vs 3 × IFNAR-/-IAV AMs vs 3 × WT IAV-SP vs 2 × WT-PBS-SPGroups 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)
Tissue-resident macrophages may be trained to confer enhanced response to heterologous re-stimulation, and thus foster versatile trained immunity (TI) against both infections and tumors. However, key priming signals that contribute to such functional versatility in trained macrophages remain not fully understood. Here we show that influenza A virus (IAV) infection in mice induces lasting transcriptional imprints of acute type-I interferon (IFN-I) signaling in lung-resident alveolar macrophages (AMs) that confer balanced anti-bacterial and anti-tumor TI responses.
Read the full summary ↓
In both IAV-infected mice and an ex vivo cytokine-mediated training system, IFN-I signaling is found to be critical to developing anti-tumor TI functions, although it limits anti-bacterial TI functions in AMs. Moreover, human AMs carrying transcriptional imprints of IFN-I signaling are associated with anti-tumor immunity and immune activation in lung cancer tissues. Our findings highlight IFN-I as a key priming signal required to developing versatile TI functions in AMs with balanced anti-bacterial and anti-tumor potential.
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 GSE295483_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 PRJNA1254769 and SRA study SRP580848. Searching any of these in the dataset finder brings you back here.

Study design
3 × IFNAR-/-PBS AMs vs 3 × IFNAR-/-IAV AMs vs 3 × WT IAV-SP vs 2 × WT-PBS-SP

Supports a between-group comparison across 11 samples.

How we read this: 4 replicated groups read from 19 sample titles; they account for 11 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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