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NLRP1 inflammasome activation in skin equivalents reveals mechanistic insights into the roles of keratinocytes in psoriasis

GSE282206 Homo sapiens (human) RNA-seq (gene expression) 24 samples Submitted 2025/09/23 Platform GPL24676
At a glance

RNA-seq (gene expression) · human · 24 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
24 samples: 8 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)
Psoriasis is a common inflammatory disease that affects mainly the skin. The pro-inflammatory cytokines interleukin(IL)-1β and IL-36γ are involved in its pathogenesis. However, the molecular and cellular mechanisms underlying the regulation of these pathways in psoriasis are incompletely understood. IL-1β activity is produced downstream of a group of protein complexes termed inflammasomes, which are primarily expressed by immune cells.
Read the full summary ↓
To address the function of the NLRP1 inflammasome in epidermal keratinocytes, we activated NLRP1 pharmacologically in human skin equivalents (SEs), an organotypic three-dimensional skin model. In the epidermis of these SEs, IL-1β secretion induced a histological phenotype that resembles psoriasis and is associated with a characteristic pro-inflammatory gene expression signature, including the induction of IL-36γ expression and secretion. Whereas expression of IL-36γ is induced by IL-1β, IL-36γ secretion occurs downstream of NLRP1 activation through gasdermin D pores. Most importantly, we detected inflammasome activation in suprabasal keratinocytes in lesional psoriasis. Release of endogenous double stranded (ds) RNA to the cytoplasm is associated with cellular perturbations in several inflammatory conditions, including psoriasis. In keratinocytes in monoculture, we identified short self-derived dsRNA as a novel activator of the NLRP1 inflammasome. These data suggest a critical role of keratinocytes in the pathogenesis of psoriasis through activation of the NLRP1 inflammasome. Furthermore, NLRP1-activated SEs represent a novel in vitro model for this condition, based on human primary skin cells. Most importantly, pharmacological targeting and inhibition of NLRP1 appears as a novel treatment option for psoriasis.
This dataset
Open GSE282206 in finder → Find more human RNA-seq datasets →
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 GSE282206_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 PRJNA1187582. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗
Study design
8 conditions, mostly in triplicate
Dermis, ASC knockout, Talabostat, ×3 Epidermis, ASC knockout, Talabostat, ×3 Dermis, ASC knockout, untreated, ×3 Epidermis, ASC knockout, untreated, ×3 Dermis, wild-type, Talabostat, ×3 Epidermis, wild-type, Talabostat, ×3 Dermis, wild-type, untreated, ×3 Epidermis, wild-type, untreated, ×3

Supports a case/control comparison: 6 samples read as cases, 6 as controls.

How we read this: 8 replicated groups read from 24 sample titles; they account for 24 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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