GEO series
Diseaase context dictates the cellular targets of IL-17 in inflammatory skin disease [2]
GSE341985
Mus musculus
Expression profiling by high throughput sequencing
27 samples
Submitted 2026/08/07
Platform GPL24247
Summary
Therapeutic blockade of IL-17 and TNF can effectively treat inflammatory skin diseases such as hidradenitis suppurativa and psoriasis, yet the relative importance of the different cell types that respond to IL-17 and TNF remains unresolved. Keratinocytes are viewed as the dominant effector cells, whereas fibroblasts have recently emerged as important contributors. In mice, topical imiquimod induces IL-17- and TNF-dependent skin inflammation and is frequently used to model psoriasis. Here, we demonstrate that intradermal injection of recombinant IL-17 and TNF elicits skin inflammation with features of hidradenitis suppurativa, including a gene expression program that is distinct from psoriasis and imiquimod-induced inflammation. Single-cell transcriptomic network analysis identified dermal fibroblasts as the dominant cell communication hub in hidradenitis suppurativa and in mice injected with IL-17 and TNF. In contrast, fibroblasts and keratinocytes both show strong network involvement in psoriasis and in mice challenged with imiquimod. Cell-type-specific deletion of IL-17 receptor A in mice revealed that imiquimod-induced inflammation depends equally on IL-17 signaling in fibroblasts and keratinocytes, whereas inflammation induced by intradermal IL-17 and TNF only requires fibroblasts to recognize IL-17 and is independent of keratinocyte IL-17 sensing. Single-cell transcriptomic analysis of these conditional knockout mice further demonstrated that keratinocytes and fibroblasts activate divergent and disease-dependent transcriptional programs following activation by IL-17. Together, these findings introduce a new conceptual framework wherein IL-17 signaling is routed through distinct cellular and molecular pathways depending on disease context and establish complementary experimental systems for interrogating type 17 skin inflammation.
This dataset
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Direct links to NCBI, no account and no request form: the whole study as GSE341985_RAW.tar, processed values as the series matrix, the supplementary file directory, and per-sample supplementary files for any of the 27 samples. Raw sequencing reads are also available from ENA.
Also filed as BioProject PRJNA1504959 and SRA study SRP722860. Searching any of these in the dataset finder brings you back here.
Study design
15 × 13893-JF vs 12 × 13894-JF
Supports a between-group comparison across 27 samples.
2 replicated groups read from 27 sample titles; they account for 27 of them. Check it against the sample list below before relying on it.
Samples in this study
0 selected
- GSM9921350 13894-JF-10
- GSM9921351 13894-JF-11
- GSM9921352 13894-JF-12
- GSM9921353 13894-JF-13
- GSM9921354 13894-JF-14
- GSM9921355 13894-JF-15
- GSM9921356 13894-JF-1
- GSM9921357 13894-JF-2
- GSM9921358 13894-JF-3
- GSM9921359 13894-JF-5
- GSM9921360 13894-JF-6
- GSM9921361 13894-JF-7
- GSM9921362 13893-JF-1
- GSM9921363 13893-JF-2
- GSM9921364 13893-JF-3
- GSM9921365 13893-JF-4
- GSM9921366 13893-JF-5
- GSM9921367 13893-JF-6
- GSM9921368 13893-JF-7
- GSM9921369 13893-JF-8
- GSM9921370 13893-JF-9
- GSM9921371 13893-JF-10
- GSM9921372 13893-JF-11
- GSM9921373 13893-JF-12
- GSM9921374 13893-JF-13
- GSM9921375 13893-JF-14
- GSM9921376 13893-JF-15
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