Evidence map›Paper›PMID 21148126›Full record

ArticleScience translational medicine2010

Gene from a psoriasis susceptibility locus primes the skin for inflammation.

Ronald Wolf, Francesca Mascia, Alif Dharamsi, O M Zack Howard, Christophe Cataisson, Val Bliskovski, Jason Winston, Lionel Feigenbaum, Ulrike Lichti, Thomas Ruzicka and 2 more

Open access · greenAbstract read
In one paragraph

Article in Science translational medicine, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
3.3field-weighted citation impact, top 7% 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

37 citing papers in PubMed, 82 citations in OpenAlex.

  1. Trial
  2. Exacerbation of inflammatory bone loss in TET2-driven clonal hematopoiesis.Journal of immunology (Baltimore, Md. : 1950) · 2026
    Article
  3. Review
  4. Linear psoriasis and Koebner phenomenon: A review.Journal of research in medical sciences : the official journal of Isfahan University of Medical Sciences · 2026
    Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Pathogenic role of S100 proteins in psoriasis.Frontiers in immunology · 2023
    Review
  10. Review
  11. Psoriatic arthritis from a mechanistic perspective.Nature reviews. Rheumatology · 2022
    Review
  12. Article
  13. Article
  14. Purinergic Signaling and Inflammasome Activation in Psoriasis Pathogenesis.International journal of molecular sciences · 2021
    Review
  15. Article
  16. Review
  17. Biotechnologically ProducedFrontiers in pharmacology · 2021
    Article
  18. Review
  19. S100 proteins in rheumatic diseases.Nature reviews. Rheumatology · 2018
    Review
  20. Article
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

12 authors at 3 institutions in 2 countries.

Ronald WolfLaboratory of Cancer Biology and Genetics, Center for Cancer Research, National Cancer Institute, Bethesda, MD 20892, USA.
Francesca Mascia
Alif Dharamsi
O M Zack Howard
Christophe Cataisson
Val Bliskovski
Jason Winston
Lionel Feigenbaum
Ulrike Lichti
Thomas Ruzicka
Triantafyllos Chavakis
Stuart H Yuspa
Center for Cancer Research · USNational Cancer Institute · USLudwig-Maximilians-Universität München · DE

Funding

Interacting Signaling Pathways that Initiate Squamous Cell CarcinogenesisZIABC004504 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI YUSPA, STUART H. · 2009 to 2022
$15.7M
MODEL SYSTEMS FOR THE STUDY OF CHEMICAL CARCINOGENESIS AT THE CELLULAR LEVELZ01BC004504 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI YUSPA, STUART H. · 1996 to 2008
$2.3M
Intramural NIH HHS Z01 BC004504
6 · The paper itself

Abstract

Psoriasis is a common complex genetic disease characterized by hyperplasia and inflammation in the skin; however, the relative contributions of epidermal cells and the immune system to disease pathogenesis remain unclear. Linkage studies have defined a psoriasis susceptibility locus (PSORS4) on 1q21, the epidermal differentiation complex, which includes genes for small S100 calcium-binding proteins. These proteins are involved in extracellular and intracellular signaling during epithelial host defense, linking innate and adaptive immunity. Inflammation-prone psoriatic skin constitutively expresses elevated concentrations of S100A7 (psoriasin) and S100A15 (koebnerisin) in the epidermis. Here, we report that genetically modified mice expressing elevated amounts of doxycycline-regulated mS100a7a15 in skin keratinocytes demonstrated an exaggerated inflammatory response when challenged by exogenous stimuli such as abrasion (Koebner phenomenon). This immune response was characterized by immune cell infiltration and elevated concentrations of T helper 1 (T(H)1) and T(H)17 proinflammatory cytokines, which have been linked to the pathogenesis of psoriasis and were further amplified upon challenge. Both inflammation priming and amplification required mS100a7a15 binding to the receptor of advanced glycation end products (RAGE). mS100a7a15 potentiated inflammation by acting directly as a chemoattractant for leukocytes, further increasing the number of inflammatory cells infiltrating the skin. This study provides a pathogenetic psoriasis model using a psoriasis candidate gene to link the epidermis and innate immune system in inflammation priming, highlighting the S100A7A15-RAGE axis as a potential therapeutic target.

Indexed as

AnimalsCells, CulturedCytokinesGenetic Predisposition to DiseaseHumansInflammationKeratinocytesMiceMice, TransgenicPsoriasisReceptor for Advanced Glycation End ProductsReceptors, ImmunologicS100 Calcium Binding Protein A7S100 ProteinsSkinTumor Necrosis Factor-alphaCytokinesReceptor for Advanced Glycation End ProductsReceptors, ImmunologicS100A7 protein, humanS100 Calcium Binding Protein A7S100 ProteinsTumor Necrosis Factor-alpha

Identifiers

PMID21148126
PMCPMC6334290
OpenAlexW2099731455

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.