GEO series

Integrative responses to IL-17 and TNF-α in human keratinocytes account for key inflammatory pathogenic circuits in psoriasis

GSE24767 Homo sapiens (human) Expression microarray 22 samples Submitted 2010/11/24 Platform GPL6947

At a glance

Expression microarray · human · 22 samples

What it is: Expression microarrayGene activity read on a chip (the older technology that RNA-seq replaced).
Organism: Homo sapiens (human)
Samples: 22 samples
Data you can get: A processed expression table (series matrix) and the array files, from NCBI.

Summary (written by the submitters)

We sought to provide a comprehensive evaluation of the effects of TNF-α and IL-17 on the keratinocyte gene profile in order to identify genes that might be co-regulated by these cytokines. We then sought to determine how genes that were synergistically activated by both cytokines relate to the psoriasis transcriptome. Here, we identified 160 unique genes that were synergistically up-regulated by IL-17 and TNF-α and 188 unique genes where the two cytokines had at least an additive effect.

Read the full summary ↓

Among highly up-regulated genes were those involved in neutrophil and lymphocyte chemotaxis, inflammation, and epidermal differentiation. Synergistically up-regulated genes included some of the highest expressed genes in lesional psoriatic skin with an impressive correlation between IL-17/TNF-α induced genes and the psoriasis gene signature. In conclusion, keratinocytes may be key drivers of pathogenetic inflammatory circuits in psoriasis through integrating responses to TNF-α and IL-17. This may explain high efficacy of targeting psoriasis with either anti-TNF-α or agents that block Th17 T-cells/IL-17 and has important implications for the development of new therapeutic agents.

This dataset

Open GSE24767 in finder → Find more human microarray datasets →

Download · which file do I need?

Direct links to NCBI, 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.

All supplementary files ↗

3 · The original raw files

Whole study · RAW.tar

Everything the authors deposited as one archive (GSE24767_RAW.tar), including the raw array or instrument files. Can be large; the picker in step 2 takes just the samples you need.

Whole study · RAW.tar ↓

What the files usually look like: For arrays the series matrix is normally the normalised expression table you want; the raw array files (CEL and similar) are in the RAW.tar.

Also filed as BioProject PRJNA132211. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 21085185) ↗

Samples in this study

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+ 22 more — browse all 22 samples with per-sample file links →

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GSE285099 RNA sequencing of human airway epithelial cultures from cystic fibrosis (CF) and non-CF donors exposed to tumor necrosis factor-alpha and interleukin-17 (TNFα+IL-17) for 5 hours 24 samples shares il-17, tnf
GSE287022 Cutaneous adipose tissue has a strong inflammatory signature in psoriasis patients, and it is partly IL-17 dependent. 241 samples shares il-17, psoriasis
GSE309097 Dynamic neutrophil-keratinocyte communication network centered on IL-36/TNFSF15 responses characterizes inflammatory responses in generalized pustular psoriasis. 17 samples shares tnf, psoriasis
GSE212836 Comparative Molecular Analysis of IL-17A and IL-23 Pathway Inhibition in Moderate-to-Severe Psoriasis: 4-Week Results from IXORA-R 199 samples shares il-17, psoriasis
GSE212476 Skin expression data from psoriasis patients treated with IL-17A inhibitor 40 samples shares il-17, psoriasis

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