ArticleThe Journal of investigative dermatology2018
Extracellular ATP and IL-23 Form a Local Inflammatory Circuit Leading to the Development of a Neutrophil-Dependent Psoriasiform Dermatitis.
Article in The Journal of investigative dermatology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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
19 citing papers in PubMed, 36 citations in OpenAlex.
- Nanozymes for ATP/cAMP balance restoration and ROS scavenging in inflammatory dermatosis treatment and recurrence prevention.Journal of nanobiotechnology · 2026Article
- A review of core immuno-inflammatory mechanisms and key regulatory targets in psoriasis.American journal of clinical and experimental immunology · 2026Review
- P2X7 a new therapeutic target to block vesicle-dependent metastasis in colon carcinoma: Role of the A2A/CD39/CD73 axis.Cell death & disease · 2025Article
- Ponatinib-induced psoriasis treated with tildrakizumab.JAAD case reports · 2025Article
- Psoriasiform Dermatitis: From Pathogenesis to New Therapeutic Opportunities.Life (Basel, Switzerland) · 2025Review
- Resident memory T cells in dirty mice suppress innate cell activation and infiltration into the skin following stimulation with alarmins.bioRxiv : the preprint server for biology · 2024Article
- Sensory ASIC3 channel exacerbates psoriatic inflammation via a neurogenic pathway in female mice.Nature communications · 2024Article
- Adenosine and Its Receptors in the Pathogenesis and Treatment of Inflammatory Skin Diseases.International journal of molecular sciences · 2024Review
- From the Skin to Distant Sites: T Cells in Psoriatic Disease.International journal of molecular sciences · 2023Review
- Chromatin accessibility and transcriptome integrative analysis revealed AP-1-mediated genes potentially modulate histopathology features in psoriasis.Clinical epigenetics · 2022Article
- Mouse Models of Psoriasis: A Comprehensive Review.The Journal of investigative dermatology · 2022Review
- P2X7 Receptor Expression and Signaling on Dendritic Cells and CD4Frontiers in cell and developmental biology · 2022Article
- Monocyte-derived and M1 macrophages from ankylosing spondylitis patients released higher TNF-α and expressed more IL1B in response to BzATP than macrophages from healthy subjects.Scientific reports · 2021Article
- Dysregulation of Connexin Expression Plays a Pivotal Role in Psoriasis.International journal of molecular sciences · 2021Article
- The Role of NLRP1, NLRP3, and AIM2 Inflammasomes in Psoriasis: Review.International journal of molecular sciences · 2021Review
- Update of P2X receptor properties and their pharmacology: IUPHAR Review 30.British journal of pharmacology · 2021Review
- Inflammasomes in Common Immune-Related Skin Diseases.Frontiers in immunology · 2020Review
- mTORC2 deficiency in cutaneous dendritic cells potentiates CD8American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2019Article
- ATP and Its Metabolite Adenosine as Regulators of Dendritic Cell Activity.Frontiers in immunology · 2018Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Psoriasis is a chronic inflammatory skin disease dependent on the IL-23/IL-17 axis, a potent inflammatory pathway involved in pathogen clearance and autoimmunity. Several triggers have been proposed as initiators for psoriasis, including alarmins such as adenosine triphosphate. However, the role of alarmins in psoriasis pathogenesis and cutaneous inflammation has not been well addressed. Studies show that signaling through the P2X7 receptor (P2X7R) pathway underlies the development of psoriasiform inflammation. In this regard, psoriasiform dermatitis induced by IL-23 is dependent on P2X7R signaling. Furthermore, direct activation of the P2X7R is sufficient to induce a well-characterized psoriasiform dermatitis. Mechanistic studies determined that P2X7R-induced inflammation is largely dependent on the IL-1β/NLRP3 inflammasome pathway and neutrophils. In conclusion, this work provides basic mechanistic insight into local inflammatory circuits induced after purinergic P2X7R signaling that are likely involved in the pathogenesis of many inflammatory diseases, such as psoriasis.
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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.