Evidence map›Paper›PMID 30377293›Full record

ArticleCell death & disease2018

IL-38 has an anti-inflammatory action in psoriasis and its expression correlates with disease severity and therapeutic response to anti-IL-17A treatment.

Laura Mercurio, Martina Morelli, Claudia Scarponi, Elan Z Eisenmesser, Nunzianna Doti, Gianluca Pagnanelli, Emanuela Gubinelli, Cinzia Mazzanti, Andrea Cavani, Menotti Ruvo and 3 more

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
79citing papers in PubMed, 1 pooled it
5.8field-weighted citation impact, top 3% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

79 citing papers in PubMed, 1 synthesis or guideline pooled it, 127 citations in OpenAlex.

  1. Pooled it
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  3. Article
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  5. Article
  6. Article
  7. Review
  8. Article
  9. Review
  10. Review
  11. Article
  12. The Immunology of Psoriasis-Current Concepts in Pathogenesis.Clinical reviews in allergy & immunology · 2024
    Review
  13. Review
  14. Article
  15. Article
  16. Interleukin-38 and Insulin Resistance.Endocrine, metabolic & immune disorders drug targets · 2024
    Article
  17. Article
  18. IL-38 regulates intestinal stem cell homeostasis by inducing WNT signaling and beneficial IL-1β secretion.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  19. The emerging role of IL-38 in diseases: A comprehensive review.Immunity, inflammation and disease · 2023
    Review
  20. Article

19 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

13 authors at 5 institutions in 3 countries.

Laura MercurioLaboratory of Experimental Immunology and Integrated Research Center for PSOriasis (CRI-PSO), Istituto Dermopatico dell'Immacolata IDI-IRCCS, via Monti di Creta, 104, ROME, Italy.
Martina MorelliLaboratory of Experimental Immunology and Integrated Research Center for PSOriasis (CRI-PSO), Istituto Dermopatico dell'Immacolata IDI-IRCCS, via Monti di Creta, 104, ROME, Italy.
Claudia ScarponiLaboratory of Experimental Immunology and Integrated Research Center for PSOriasis (CRI-PSO), Istituto Dermopatico dell'Immacolata IDI-IRCCS, via Monti di Creta, 104, ROME, Italy.
Elan Z EisenmesserDepartment of Biochemistry & Molecular Genetics, School of Medicine, University of Colorado Denver, Anschutz Campus, Aurora, 80045, CO, USA.
Nunzianna DotiIstituto di Biostrutture e Bioimmagini-CNR and CIRPEB, Via Mezzocannone, 16, Naples, 80134, Italy.
Gianluca Pagnanelli1st Division of Dermatology and CRI-PSO, Istituto Dermopatico dell'Immacolata IDI-IRCCS, via Monti di Creta, 104, Rome, 00167, Italy.
Emanuela GubinelliCRI-PSO Istituto Dermopatico dell'Immacolata, IDI-IRCCS, via Monti di Creta, 104, Rome, 00167, Italy.
Cinzia Mazzanti1st Division of Dermatology and CRI-PSO, Istituto Dermopatico dell'Immacolata IDI-IRCCS, via Monti di Creta, 104, Rome, 00167, Italy.
Andrea CavaniINMP/NIHMP, via di S.Gallicano, 25, Rome, 00153, Italy.
Menotti RuvoIstituto di Biostrutture e Bioimmagini-CNR and CIRPEB, Via Mezzocannone, 16, Naples, 80134, Italy.ORCID http://orcid.org/0000-0001-5997-756X
Charles A DinarelloDepartment of Medicine, Radboud University Medical Center, 6525 HP, Nijmegen, The Netherlands.
Cristina AlbanesiLaboratory of Experimental Immunology and Integrated Research Center for PSOriasis (CRI-PSO), Istituto Dermopatico dell'Immacolata IDI-IRCCS, via Monti di Creta, 104, ROME, Italy.ORCID http://orcid.org/0000-0002-7537-6833
Stefania MadonnaLaboratory of Experimental Immunology and Integrated Research Center for PSOriasis (CRI-PSO), Istituto Dermopatico dell'Immacolata IDI-IRCCS, via Monti di Creta, 104, ROME, Italy. s.madonna@idi.it.
Istituto Dermopatico dell'Immacolata · ITInstitute of Biostructure and Bioimaging · ITRadboud University Nijmegen · NLUniversity of Colorado Denver · USUniversity of Verona · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

IL-36 cytokines, a subgroup of IL-1 family, comprise IL-36α, IL-36β, and IL-36γ agonists, abundantly expressed in psoriatic skin, and IL-36RA and IL-38 antagonists. In psoriatic skin, IL-36 cytokines interfere with keratinocyte cornification programs and induce the release of antimicrobial peptides and chemokines active on neutrophils and Th17 lymphocytes. To date, the role of IL-38 antagonist in psoriasis remains to be defined. Here, we demonstrate that skin and circulating IL-38 levels are reduced in psoriatic patients and in other skin diseases characterized by neutrophilic infiltrate. In psoriasis, the balance of IL-36γ agonist/IL-38 antagonist serum levels is in favor of agonists and is closely associated with disease severity. Interestingly, IL-38 is upregulated by anti-IL-17A biological treatment and positively correlates with the therapeutic efficacy of secukinumab in psoriatic patients. The downregulation of IL-38 expression is strictly related to keratinocyte de-differentiation triggered by the inflammatory cytokines IL-36γ, IL-17, and IL-22. Finally, we demonstrate that administration of recombinant full-length IL-38 counteracts in vitro the biological processes induced by IL-36γ in human keratinocytes and endothelial cells and attenuates in vivo the severity of the psoriasiform phenotype induced by IMQ in mice. Such effects are achieved by restoring the physiological programs of keratinocyte proliferation and differentiation, and reducing the immune cell infiltrates.

Indexed as

AdolescentAdultAgedAnimalsAntibodies, Monoclonal, HumanizedCase-Control StudiesDisease Models, AnimalEndothelial CellsFemaleGene Expression RegulationHumansImiquimodImmunologic FactorsInterleukin-1Interleukin-17InterleukinsAntibodies, Monoclonal, HumanizedIL17A protein, humanIL1RL2 protein, humanIL36G protein, humanIL-38 protein, humanImiquimodImmunologic FactorsInterleukin-1Interleukin-17InterleukinsReceptors, Interleukin-1secukinumab

Identifiers

PMID30377293
PMCPMC6207563
OpenAlexW2899084465

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.