GEO series
Targeting JAK1/3-STAT1 signaling attenuates cytotoxic T lymphocytes activation for the treatment in Stevens-Johnson syndrome and toxic epidermal necrolysis
GSE333617
Homo sapiens
Expression profiling by high throughput sequencing; Other
26 samples
Submitted 2026/06/25
Platform GPL24676
Summary
Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) are life-threatening severe cutaneous adverse reactions (SCARs). We integrate single-cell and spatial transcriptomic analyses on blood, blisters, and lesional skin from SJS/TEN patients, revealing IFN-γ and JAK/STAT signaling as the key pathways responsible for driving epidermal necrolysis. We identify JAK1/3–STAT1 signaling as a primary driver of the activation of CD8+ cytotoxic T lymphocytes (CTLs), natural killer (NK)/NKT cells, macrophages and conventional dendritic cells in skin lesions. The high proportion of cytotoxic protein (granulysin and granzyme B)–expressing CD8+ CTLs in SJS/TEN blisters is associated with STAT1 phosphorylation. Immunostaining and ex vivo blocking assays further confirm the potential for the JAK1/3 inhibitor to attenuate CD8+ CTL activation in SJS/TEN. We conduct a proof-of-concept clinical trial in 20 patients with SJS/TEN (ClinicalTrials.gov: NCT06474078), and find that the JAK1/3 inhibitor tofacitinib improves clinical outcomes by reducing skin-healing time with no observed mortality. Our study provides an effective and alternative mechanism-based therapeutic approach for SJS/TEN.
This dataset
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Direct links to NCBI, no account and no request form: the whole study as GSE333617_RAW.tar, processed values as the series matrix, the supplementary file directory, and per-sample supplementary files for any of the 26 samples. Raw sequencing reads are also available from ENA.
Also filed as BioProject PRJNA1471675 and SRA study SRP704506. Searching any of these in the dataset finder brings you back here.
Study design
26 conditions, each sampled once — no replicated groups
Read from 26 sample titles: 26 distinct titles with little repetition. Check it against the sample list below before relying on it.
Samples in this study
0 selected
- GSM9769897 HD43_PBMC; HD4 [GEX]
- GSM9769898 HD43_PBMC; HD4 [TCR]
- GSM9769899 AdrD1150_BC; STB1 [TCR]
- GSM9769900 AdrD5833_BC; STB2 [GEX]
- GSM9769901 AdrD5833_BC; STB2 [TCR]
- GSM9769902 AdrD8172_BC; STB3 [TCR]
- GSM9769903 AdrD9316_BC; STB4 [TCR]
- GSM9769904 AdrD9712_BC; STB7 [GEX]
- GSM9769905 AdrD9712_BC; STB7 [TCR]
- GSM9769906 AdrD9292_BC, AdrD9292_PBMC; STB5, STP5 [CSP]
- GSM9769907 AdrD9292_BC, AdrD9292_PBMC; STB5, STP5 [GEX]
- GSM9769908 AdrD9292_BC, AdrD9292_PBMC; STB5, STP5 [TCR]
- GSM9769909 AdrD10022_BC, AdrD10022_PBMC; STB6, STP6 [CSP]
- GSM9769910 AdrD10022_BC, AdrD10022_PBMC; STB6, STP6 [GEX]
- GSM9769911 AdrD10022_BC, AdrD10022_PBMC; STB6, STP6 [TCR]
- GSM9769912 AdrD1150_PBMC, AdrD5833_2_PBMC, AdrD8172_PBMC; STP1, STP2, STP3 [TCR]
- GSM9769913 AdrD9316_PBMC, AdrD9316_10_PBMC; STP4, STP4_post [TCR]
- GSM9769914 AdrD9292_10_PBMC, AdrD10022_13_PBMC; STP5_post, STP6_post [CSP]
- GSM9769915 AdrD9292_10_PBMC, AdrD10022_13_PBMC; STP5_post, STP6_post [GEX]
- GSM9769916 AdrD9292_10_PBMC, AdrD10022_13_PBMC; STP5_post, STP6_post [TCR]
- GSM9769917 skin_HD13, skin_HD14, skin_HD15; HD27_skin, HD28_skin, HD29_skin [CSP]
- GSM9769918 skin_HD13, skin_HD14, skin_HD15; HD27_skin, HD28_skin, HD29_skin [GEX]
- GSM9769919 AdrD11588_skinV; SJS24_spatial
- GSM9769920 AdrD11512_skinV; SJS33_spatial
- GSM9769921 HD4_skinV; HD30_spatial
- GSM9769922 HD8HD9_skinV; HD31HD32_spatial
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