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Differential response of human plasmacytoid pre-dendritic cells to SARS-CoV-2 variants

GSE294888 Homo sapiens (human) RNA-seq (gene expression) 40 samples Submitted 2025/06/01 Platform GPL24676
At a glance

RNA-seq (gene expression) · human · 40 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
40 samples: 8 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.
Summary (written by the submitters)
SARS-CoV-2 variants have been involved in various waves of the COVID19 pandemic and showed different pathogenicity and inflammatory potential. Whether they can induce different patterns of innate immune activation in antigen-presenting cells is poorly understood. Here, we investigated the ability of primary plasmacytoid pre-dendritic cells (pDC), type 2 dendritic cells (DC2), and monocytes isolated from healthy blood donors to respond to SARS-CoV-2 variants.
Read the full summary ↓
Transcriptomic profiling using RNA sequencing revealed that pDC respond differentially to SARS-CoV-2 variants, while DC2 and monocytes do not. Functional studies showed that pDC undergo differential activation programs upon SARS-CoV-2 variant stimulation. The Alpha B220/95 and Delta variants induced P1-/P2-pDC effector phenotypes, characterized by strong IFN-α production. On the contrary, BA.1 variant turned pDC into a predominant T cell activating P3 phenotype, with less IFN-α and IFN-λ production, and stronger proinflammatory and CD4+T cell responses. Our results indicate that pDC activation and diversification pattern can be differentially controlled by SARS-CoV-2 variants, which may influence disease severity
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 GSE294888_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 PRJNA1251981 and SRA study SRP579389. Searching any of these in the dataset finder brings you back here.

Study design
8 conditions, mostly with about 5 replicates each
pDC,NI, ×5 pDC,R848, ×5 pDC,Delta, ×5 pDC,BA.1, ×5 DC2,NI, ×5 DC2,R848, ×5 DC2,Delta, ×5 DC2,BA.1, ×5

Supports a between-group comparison across 40 samples.

How we read this: 8 replicated groups read from 40 sample titles; they account for 40 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.