ArticleNature communications2025
Dynamic neutrophil-keratinocyte communication network centered on IL-36/TNFSF15 responses characterizes inflammatory responses in generalized pustular psoriasis.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
5 citing papers in PubMed.
- Matrix Metalloproteinase-9 (MMP-9) in Psoriasis: Integrating Extracellular Matrix Remodeling, Neutrophil-Endothelial Crosstalk and Biomarker Evidence.Medical sciences (Basel, Switzerland) · 2026Review
- IL-36-Driven Inflammation in Generalized Pustular Psoriasis: Immunological Insights from Plaque Psoriasis and Implications for Targeted Therapy.International journal of molecular sciences · 2026Review
- TYMP upregulation mediated by the hyperactivated IL-17/NF-κB1 axis promotes psoriasis through enhancing aberrant keratinization and neutrophil-mediated inflammation.Biology direct · 2026Article
- TL1A morphological shifts and inflammatory heterogeneity in rhinosinusitis and allergic rhinitis: a hypothesis-driven review.Frontiers in immunology · 2026Review
- SAPHO syndrome and pustular skin diseases: shared inflammatory circuits, divergent tissue outcomes, and the limits of a spectrum model.Frontiers in immunology · 2026Review
Corrections and comments
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Authors and funding
21 authors.
Funding
Abstract
Generalized pustular psoriasis (GPP) is a severe subtype of psoriasis characterized by epidermal neutrophil infiltration, often presenting as acute, potentially life-threatening flares. However, the characterization of the immune micro-environment in GPP lesions remains largely unknown. Here, we use single-cell RNA profiling to interrogate the transcriptomes of 60,000 single cells from GPP lesional skin (n = 13) and healthy adult skin (n = 4), combined with spatial transcriptomics. We identify a neutrophil subset lacking CASP8 expression but exhibiting elevated levels of inflammatory pathway genes, including RIPK1, NFKB1, IL1B, CXCL1, and CXCL8 in GPP flares, illustrating neutrophil transition from pre-inflammatory to a pro-inflammatory state, and activation of a communication network between IL36G+ keratinocytes and neutrophils in GPP lesions, with TNFSF15 (TL1A) released from neutrophils exaggerating the inflammatory crosstalk. We further demonstrate that fibroblasts and capillary endothelial cells function as central communication hubs in GPP, through dynamic receptor-ligand interactions with several spatially proximate immune cells, including T cells, neutrophils, and macrophages. In this work, we provide an in-depth view of immune cell participation and highlight the role of neutrophil-keratinocyte crosstalk in GPP pathogenesis.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.