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Dissecting the molecular pathways through which long-chain PFAS disrupts dendritic cell maturation

GSE338576 Homo sapiens (human) RNA-seq (gene expression) 15 samples Submitted 2026/07/20 Platform GPL24676
At a glance

RNA-seq (gene expression) · human · 15 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
15 samples: 5 conditions, mostly in triplicateGroups 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)
Per- and polyfluoroalkyl substances (PFAS) have been associated with impaired vaccine responsiveness and altered immune function, but the mechanisms underlying their immunotoxic effects remain incompletely understood. Because dendritic cells (DCs) play a central role in antigen presentation and initiation of adaptive immunity, this study investigated the effects of selected PFAS on DC maturation and the underlying molecular pathways.
Read the full summary ↓
Human THP-1-derived DCs were exposed to four long chain PFAS followed by transcriptomic analysis, quantitative gene expression analysis, and pharmacological modulation of peroxisome proliferator-activated receptor alpha (PPARα)- and glucocorticoid receptor (GR)-associated pathways. Perfluorooctanoic acid (PFOA) induced the strongest transcriptional response, characterized by enrichment of pathways involved in fatty acid oxidation, peroxisomal metabolism, and PPAR signaling. Among the affected genes, pyruvate dehydrogenase kinase 4 (PDK4) emerged as a robust marker of PFAS-induced metabolic reprogramming. Functionally, PFAS exposure reduced expression of HLA-DR isotype, a key marker of DC maturation, with PFOA showing greater potency than the other compounds tested. Pharmacological inhibition experiments demonstrated that both PPARα-associated and GR-associated mechanisms contribute to the observed phenotype, although neither pathway alone fully accounted for the impairment. Overall, these findings indicate that PFAS disrupt DC maturation through coordinated immunometabolic reprogramming involving interconnected nuclear receptor signaling pathways, providing mechanistic support for the immunotoxic effects associated with PFAS exposure.
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 GSE338576_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 PRJNA1495195 and SRA study SRP717913. Searching any of these in the dataset finder brings you back here.

Study design
5 conditions, mostly in triplicate
immature DCs, 24h, control, ×3 immature DCs, 24h, PFOA , ×3 immature DCs, 24h, PFOS , ×3 immature DCs, 24h, dexamethasone , ×3 immature DCs, 24h, GW7647, ×3

Supports a between-group comparison across 15 samples.

How we read this: 5 replicated groups read from 15 sample titles; they account for 15 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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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.