Evidence map›Paper›PMID 29316717›Full record

ReviewInternational journal of molecular sciences2018

Scanning the Immunopathogenesis of Psoriasis.

Andrea Chiricozzi, Paolo Romanelli, Elisabetta Volpe, Giovanna Borsellino, Marco Romanelli

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 145 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
145citing papers in PubMed, 1 pooled it
13.1field-weighted citation impact, top 1% 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

145 citing papers in PubMed, 1 synthesis or guideline pooled it, 313 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Skewed MHC Class I Peptide Presentation in Psoriatic Arthritis.International journal of molecular sciences · 2026
    Article
  4. Article
  5. Review
  6. NMI promotes the secretion of IL-17 and exacerbates psoriasis.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. The Role of Selected Proteins in the Pathogenesis of Psoriasis.International journal of molecular sciences · 2025
    Review
  19. Article
  20. Review

85 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

5 authors at 3 institutions in 2 countries.

Andrea ChiricozziDermatology Department, University of Pisa, Via Roma 67, 56126 Pisa, Italy. andrea.chiricozzi@unipi.it.
Paolo RomanelliDepartment of Dermatology and Cutaneous Surgery, University of Miami Miller School of Medicine, 1295 NW 14th St, Miami, FL 33125, USA. promanelli@med.miami.edu.
Elisabetta VolpeThe Laboratory of Neuroimmunology, Fondazione Santa Lucia, Via del Fosso di Fiorano, 64, 00143 Rome, Italy. e.volpe@hsantalucia.it.ORCID 0000-0001-7985-2422
Giovanna BorsellinoThe Laboratory of Neuroimmunology, Fondazione Santa Lucia, Via del Fosso di Fiorano, 64, 00143 Rome, Italy. g.borsellino@hsantalucia.it.
Marco RomanelliDermatology Department, University of Pisa, Via Roma 67, 56126 Pisa, Italy.
Fondazione Santa Lucia · ITUniversity of Pisa · ITUniversity of Miami · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Psoriasis is a chronic inflammatory skin disease, the immunologic model of which has been profoundly revised following recent advances in the understanding of its pathophysiology. In the current model, a crosstalk between keratinocytes, neutrophils, mast cells, T cells, and dendritic cells is thought to create inflammatory and pro-proliferative circuits mediated by chemokines and cytokines. Various triggers, including recently identified autoantigens, Toll-like receptor agonists, chemerin, and thymic stromal lymphopoietin may activate the pathogenic cascade resulting in enhanced production of pro-inflammatory and proliferation-inducing mediators such as interleukin (IL)-17, tumor necrosis factor (TNF)-α, IL-23, IL-22, interferon (IFN)-α, and IFN-γ by immune cells. Among these key cytokines lie therapeutic targets for currently approved antipsoriatic therapies. This review aims to provide a comprehensive overview on the immune-mediated mechanisms characterizing the current pathogenic model of psoriasis.

Indexed as

AnimalsCytokinesDendritic CellsHumansLymphocytesPsoriasisCytokinesautoantigenautoreactive T cellschemokinescytokinesdendritic cellsIL-17IL-23immunologypathogenesispsoriasis

Identifiers

PMID29316717
PMCPMC5796128
OpenAlexW2783502763

What Socratic 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 Socratic graph.