Evidence map›Paper›PMID 26215033›Full record

ReviewJournal of autoimmunity2015

The immunogenetics of Psoriasis: A comprehensive review.

Jamie L Harden, James G Krueger, Anne M Bowcock

Abstract readReview
In one paragraph

Review in Journal of autoimmunity, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 256 papers, 6 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
256citing papers in PubMed, 6 pooled it
23.4field-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

256 citing papers in PubMed, 6 syntheses or guidelines pooled it, 593 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
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  4. Pooled it
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  6. Pooled it
  7. Trial
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  11. Indirect Regulation and Equilibrium of p35 and p40 Subunits of Interleukin (IL)-12/23 by Ustekinumab in Psoriasis Treatment.Medical science monitor : international medical journal of experimental and clinical research · 2020
    Trial
  12. Trial
  13. Trial
  14. Article
  15. Article
  16. Shared Pathways between Psoriasis and Atopic Dermatitis.Dermatology practical & conceptual · 2026
    Review
  17. The Effect of Ozone Therapy on Psoriasis.Clinical case reports · 2026
    Article
  18. Dissecting PGENature communications · 2026
    Article
  19. Article
  20. Review

196 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 3 institutions in 2 countries.

Jamie L HardenThe Laboratory for Investigative Dermatology, The Rockefeller University, New York, NY 10065, USA; Dermira, Inc. Menlo Park, CA 94025, USA.
James G KruegerThe Laboratory for Investigative Dermatology, The Rockefeller University, New York, NY 10065, USA.
Anne M BowcockNational Heart and Lung Institute, Imperial College, London SW3 6LY, UK. Electronic address: A.bowcock@imperial.ac.uk.
Imperial College London · GBMenlo School · USRockefeller University · US

Funding

Genome-Wide SNP Association in PsoriasisR01AR050266 · NIAMS · WASHINGTON UNIVERSITY · PI BOWCOCK, ANNE MARY · 2007 to 2016
$5.7M
Origin and Function of Inflammatory Dendritic Cells in Psoriasis.R01AR060222 · NIAMS · ROCKEFELLER UNIVERSITY · PI LOWES, MICHELLE A · 2011 to 2013
$1.1M
NIAMS NIH HHS 1R01AR060222NIAMS NIH HHS R01 AR050266NIAMS NIH HHS R01AR050266NIAMS NIH HHS R01 AR060222
6 · The paper itself

Abstract

Psoriasis vulgaris is a common, chronic inflammatory skin disease with a complex etiology involving genetic risk factors and environmental triggers. Here we describe the many known genetic predispositions of psoriasis with respect to immune genes and their encoded pathways in psoriasis susceptibility. These genes span an array of functions that involve antigen presentation (HLA-Cw6, ERAP1, ERAP2, MICA), the IL-23 axis (IL12Bp40, IL23Ap19, IL23R, JAK2, TYK2), T-cell development and T-cells polarization (RUNX1, RUNX3, STAT3, TAGAP, IL4, IL13), innate immunity (CARD14, c-REL, TRAF3IP2, DDX58, IFIH1), and negative regulators of immune responses (TNIP1, TNFAIP3, NFKBIA, ZC3H12C, IL36RN, SOCS1). The contribution of some of these gene products to psoriatic disease has also been revealed in recent years through targeting of key immune components, such as the Th17/IL-23 axis which has been highly successful in disease treatment. However, many of the genetic findings involve immune genes with less clear roles in psoriasis pathogenesis. This is particularly the case for those genes involved in innate immunity and negative regulation of immune specific pathways. It is possible that risk alleles of these genes decrease the threshold for the initial activation of the innate immune response. This could then lead to the onslaught of the pathogenic adaptive immune response known to be active in psoriatic skin. However, precisely how these various genes affect immunobiology need to be determined and some are speculated upon in this review. These novel genetic findings also open opportunities to explore novel therapeutic targets and potentially the development of personalized medicine, as well as discover new biology of human skin disease.

Indexed as

Genetic Predisposition to DiseaseImmunogeneticsAntigen PresentationGenetic LociHumansImmunity, InnateImmunomodulationPsoriasisT-Lymphocyte SubsetsGeneticsImmunologyInnate immunityNegative regulatorsPsoriasisTh17-axis

Identifiers

PMID26215033
PMCPMC4628849
OpenAlexW962657022

What OpenQuestion holds

Textmetadata
LicenceTDM
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.