GEO series

Cell-intrinsic Tim-3 is Required for Optimal CD8 Response to Acute LCMV Infection [RNAseq]

GSE300892 Mus musculus (mouse) RNA-seq (gene expression) 10 samples Submitted 2025/07/01 Platform GPL19057

At a glance

RNA-seq (gene expression) · mouse · 10 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: 10 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.

Summary (written by the submitters)

Tim-3, or transmembrane immunoglobulin and mucin domain-3, is a type I membrane protein expressed by various immune cell types and which is best known as a negative regulator of anti-tumor immunity. However, Tim-3 also has a co-stimulatory role in T cells under some conditions, via enhancement of PI3K signaling. We hypothesize that Tim-3 signaling enhances CD8+ T cell activation during acute infection and contributes to enhanced CD8+ effector function.

Read the full summary ↓

To test this hypothesis, we used LCMV-specific TCR transgenic (P14) mice expressing a truncated, non-signaling, allele of Tim-3 or CD8-specific deletion of Tim-3. CD8+ T cell effectors were analyzed by flow cytometry after acute infection with LCMV Armstrong. At the effector stage, endogenous Tim-3+ T cells had increased expression of effector CD8 markers, compared with Tim-3 negative cells. Tim-3 knockout mice also showed a significantly lower number of LCMV-specific T cells. Additionally, endogenous Tim-3+ T cells were also significantly better at cytokine production and had increased cytotoxicity. Tim-3 expression correlated with better cell survival in homeostatic conditions after the virus had been cleared. Bulk RNA sequencing and TCR sequencing revealed that Tim-3-expressing effector CD8+ T cells had a distinct pattern of effector gene upregulation, with increased expansion of a subset of TCR clones. Mechanistically, Tim-3 signals enhances phosphorylation of Foxo1, inhibiting its entry into the nucleus, conferring enhanced effector function. Thus, Tim-3 signaling contributes positively to an effective CD8+ T cell response during acute infection. These findings may lead to a better understanding of CD8+ T cell function in different settings, including in tumors.

This dataset

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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 GSE300892_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 PRJNA1282608 and SRA study SRP594843. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗

Samples in this study

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+ 10 more — browse all 10 samples with per-sample file links →

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