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Temporal modulation of gene expression in a controlled Schistosoma mansoni human infection model

GSE313156 Homo sapiens (human) RNA-seq (gene expression) 144 samples Submitted 2025/12/16 Platform GPL24676
At a glance

RNA-seq (gene expression) · human · 144 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
Homo sapiens (human)
Samples
144 samples: 30 conditions, mostly with about 5 replicates eachGroups 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
Temporal modulation of gene expression in a controlled Schistosoma mansoni human infection modelFrontiers in immunology · 2025
Summary (written by the submitters)
Background Schistosomiasis is caused by parasitic blood flukes of the genus Schistosoma. Despite ongoing mass drug administration efforts, the disease remains a major public health burden in endemic regions. A better understanding of early host responses to schistosomiasis is critical for developing effective vaccines and therapeutics.
Read the full summary ↓
Methods We conducted a longitudinal transcriptomic study of peripheral blood samples from 30 Schistosoma-naïve volunteers participating in two controlled human infection trials with male-or female-only S. mansoni cercariae. Blood was collected at six time points over 20 weeks post-infection. Whole-transcriptome RNA sequencing and integrative analyses, including differential gene expression, gene set enrichment, protein interaction networks, co-expression clustering, and immune module profiling, were employed to characterize temporal modulation of genes related to immune responses. Results Robust and highly time-dependent transcriptional responses were observed, peaking at Week 4 post-infection. Differential gene expression and pathway analyses revealed activation of immune responses, including type I and II interferon signaling, chemokine-mediated pathways, and antigen presentation. Notably, both Th1 and Th2 signatures were evident at Week 4. Key immune hubs included IFNG, TNF, and IL1B, along with transcriptional regulators such as STAT1 and IRF7. Blood transcription module analysis further highlighted transient activation of interferon and plasma cell-related responses. Conclusions This study provides a comprehensive transcriptional map of early host responses to S. mansoni infection in humans. The findings underscore the central role of interferon pathways, early mixed Th1/Th2 polarization, and inflammation-associated gene signatures in shaping host response to S. mansoni infection. These insights may inform the rational design of vaccines and biomarkers for schistosomiasis.
Published in
Temporal modulation of gene expression in a controlled Schistosoma mansoni human infection model
Li D, Jiang C, Zhu W et al. · Frontiers in immunology 2025 · PMID 41476985 · doi:10.3389/fimmu.2025.1707749
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 GSE313156_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 PRJNA1378726 and SRA study SRP654002. Searching any of these in the dataset finder brings you back here.

Study design
30 conditions, mostly with about 5 replicates each
Blood,S01_W ×6 Blood,S09_W ×6 Blood,S10_W ×6 Blood,S17_W ×6 Blood,S18_W ×6 Blood,S25_W ×6 Blood,S28_W ×6 Blood,S04_W ×5 +22 more

Supports a between-group comparison across 144 samples.

How we read this: 30 replicated groups read from 144 sample titles; they account for 144 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

+ 104 more — browse all 144 samples with per-sample file links →

Datasets on a similar topic

Search all human RNA-seq datasets in GEO →

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