ArticleThe Journal of experimental medicine2024
Human neutrophils drive skin autoinflammation by releasing interleukin (IL)-26.
Article in The Journal of experimental medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
11 citing papers in PubMed, 19 citations in OpenAlex.
- Immune shifts in inflammatory skin diseases.JID innovations : skin science from molecules to population health · 2026Review
- METTL7A-Dependent mMedComm · 2026Article
- Prevotella copri Exacerbates Psoriasis Through Keratinocyte-Neutrophil Crosstalk via NF-κB Activation.Experimental dermatology · 2026Article
- Psoriasis-like disease prevents squamous skin tumor development by neutrophil-driven inflammation.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Preparation Strategy of Hydrogel Loaded with Natural Products and Its Research Progress in Skin Repair.Gels (Basel, Switzerland) · 2026Review
- Article
- Multifaceted Roles of IL-26 in Physiological and Pathological Conditions.International journal of molecular sciences · 2025Review
- Th17 cells with regulatory phenotype are the main IL-17F and IL-26 producers in palmoplantar pustulosis.JCI insight · 2025Article
- Considerations for defining and diagnosing generalized pustular psoriasis.Journal of the European Academy of Dermatology and Venereology : JEADV · 2025Review
- The role of CEACAMs in neutrophil function.European journal of clinical investigation · 2024Review
- Current Treatments for Generalized Pustular Psoriasis: A Narrative Summary of a Systematic Literature Search.Dermatology and therapy · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 3 institutions in 3 countries.
Funding
Abstract
Autoinflammation is a sterile inflammatory process resulting from increased neutrophil infiltration and overexpression of IL-1 cytokines. The factors that trigger these events are, however, poorly understood. By investigating pustular forms of psoriasis, we show that human neutrophils constitutively express IL-26 and abundantly release it from granular stores upon activation. In pustular psoriasis, neutrophil-derived IL-26 drives the pathogenic autoinflammation process by inducing the expression of IL-1 cytokines and chemokines that further recruit neutrophils. This occurs via activation of IL-26R in keratinocytes and via the formation of complexes between IL-26 and microbiota DNA, which trigger TLR9 activation of neutrophils. Thus our findings identify neutrophils as an important source of IL-26 and point to IL-26 as the key link between neutrophils and a self-sustaining autoinflammation loop in pustular psoriasis.
Indexed as
Identifiers
What OpenQuestion holds
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.