Evidence map›Paper›PMID 29387591›Full record

ReviewPsoriasis (Auckland, N.Z.)2016

Current knowledge on psoriasis and autoimmune diseases.

Nilmarie Ayala-Fontánez, David C Soler, Thomas S McCormick

Open access · goldAbstract readReview
In one paragraph

Review in Psoriasis (Auckland, N.Z.), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 113 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
113citing papers in PubMed, 3 pooled it
5.6field-weighted citation impact, top 4% 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

113 citing papers in PubMed, 3 syntheses or guidelines pooled it, 265 citations in OpenAlex.

  1. Pooled it
  2. Frontiers in medicine · 2024
    Pooled it
  3. Pooled it
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Observational
  10. Article
  11. Review
  12. Psoriasis and Alopecia: Unveiling the Links.Dermatology practical & conceptual · 2025
    Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Review
  19. Article
  20. Article

53 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

3 authors at 2 institutions in 1 country.

Nilmarie Ayala-FontánezDepartment of Dermatology, Case Western Reserve University, Cleveland, OH, USA.
David C SolerDepartment of Dermatology, Case Western Reserve University, Cleveland, OH, USA.
Thomas S McCormickDepartment of Dermatology, Case Western Reserve University, Cleveland, OH, USA.
University Hospitals Case Medical Center · USCase Western Reserve University · US

Funding

Vitamin D endocrine system and Protection Against Skin TumorlgenesisP30AR039750 · NIAMS · CASE WESTERN RESERVE UNIVERSITY · PI COOPER, KEVIN D · 1988 to 2015
$9.1M
NIAMS NIH HHS P30 AR039750
6 · The paper itself

Abstract

Psoriasis is a prevalent, chronic inflammatory disease of the skin, mediated by crosstalk between epidermal keratinocytes, dermal vascular cells, and immunocytes such as antigen presenting cells (APCs) and T cells. Exclusive cellular "responsibility" for the induction and maintenance of psoriatic plaques has not been clearly defined. Increased proliferation of keratinocytes and endothelial cells in conjunction with APC/T cell/monocyte/macrophage inflammation leads to the distinct epidermal and vascular hyperplasia that is characteristic of lesional psoriatic skin. Despite the identification of numerous susceptibility loci, no single genetic determinant has been identified as responsible for the induction of psoriasis. Thus, numerous other triggers of disease, such as environmental, microbial and complex cellular interactions must also be considered as participants in the development of this multifactorial disease. Recent advances in therapeutics, especially systemic so-called "biologics" have provided new hope for identifying the critical cellular targets that drive psoriasis pathogenesis. Recent recognition of the numerous co-morbidities and other autoimmune disorders associated with psoriasis, including inflammatory bowel disease, multiple sclerosis, rheumatoid arthritis, and systemic lupus erythematosus suggest common signaling elements and cellular mediators may direct disease pathogenesis. In this review, we discuss common cellular pathways and participants that mediate psoriasis and other autoimmune disorders that share these cellular signaling pathways.

Indexed as

autoimmunityimmunosuppressionpsoriasis

Identifiers

PMID29387591
PMCPMC5683130
OpenAlexW2286025093

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.