Evidence map›Paper›PMID 21850017›Full record

ArticleThe Journal of investigative dermatology2012

Cathelicidin antimicrobial peptide LL-37 in psoriasis enables keratinocyte reactivity against TLR9 ligands.

Shin Morizane, Kenshi Yamasaki, Beda Mühleisen, Paul F Kotol, Masamoto Murakami, Yumi Aoyama, Keiji Iwatsuki, Tissa Hata, Richard L Gallo

Open access · greenAbstract read
In one paragraph

Article in The Journal of investigative dermatology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 93 papers.

0numbers the graph read from it
0cells of the map it votes in
93citing papers in PubMed
8.2field-weighted citation impact, top 2% 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

93 citing papers in PubMed, 223 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Review
  4. Article
  5. Review
  6. Review
  7. Review
  8. Antimicrobial Peptide Signaling in Skin Diseases.JID innovations : skin science from molecules to population health · 2025
    Review
  9. Article
  10. Review
  11. Review
  12. Review
  13. Pharmacological Management of Psoriasis: Current Landscape and Future Perspectives.Recent advances in inflammation & allergy drug discovery · 2025
    Review
  14. Review
  15. Review
  16. Review
  17. Review
  18. Article
  19. Review
  20. Article

33 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

9 authors at 4 institutions in 2 countries.

Shin MorizaneDivision of Dermatology, Department of Medicine, University of California, San Diego and VA San Diego Healthcare System, San Diego, California, USA. zanemori@cc.okayama-u.ac.jp
Kenshi Yamasaki
Beda Mühleisen
Paul F Kotol
Masamoto Murakami
Yumi Aoyama
Keiji Iwatsuki
Tissa Hata
Richard L Gallo
University of California San Diego · USOkayama University · JPAsahikawa Medical College Hospital · JPTohoku University · JP

Funding

Cathelicidins in Skin ImmunityR01AI052453 · NIAID · VETERANS MEDICAL RESEARCH FDN/SAN DIEGO · PI GALLO, RICHARD L, NIZET, VICTOR · 2002 to 2017
$5.3M
Cathelicidin in Skin ImmunityR37AI052453 · NIAID · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI Richard L Gallo, Victor Nizet · 2019 to 2026
$4.6M
Proteolysis and Skin AntimicrobialsR01AR052728 · NIAMS · VETERANS MEDICAL RESEARCH FDN/SAN DIEGO · PI GALLO, RICHARD L · 2006 to 2015
$3.3M
NIAID NIH HHS R01 AI052453NIAID NIH HHS R37 AI052453NIAMS NIH HHS R01 AR052728
6 · The paper itself

Abstract

Here we show that keratinocytes in psoriatic lesional skin express increased Toll-like receptor (TLR) 9 that similarly localizes with elevated expression of the cathelicidin antimicrobial peptide LL-37. In culture, normal human keratinocytes exposed to LL-37 increased TLR9 expression. Furthermore, when keratinocytes were exposed to LL-37 and subsequently treated with TLR9 ligands, such as CpG or genomic DNA, they greatly increased production of type I IFNs. This response mimicked observations in the epidermis of psoriatic lesional skin as keratinocytes in psoriatic lesions produce greater amounts of IFN-β than normal skin lacking LL-37. The mechanism for induction of type I IFNs in keratinocytes was dependent on TLR9 expression but not on a DNA-LL-37 complex. These findings suggest that keratinocytes recognize and respond to DNA and can actively participate in contributing to the immunological environment that characterizes psoriasis.

Indexed as

Antimicrobial Cationic PeptidesBiopsyCathelicidinsCells, CulturedCpG IslandsDNAEpidermal CellsGene ExpressionHumansInterferon-betaInterferon Type IKeratinocytesLigandsPsoriasisToll-Like Receptor 9Antimicrobial Cationic PeptidesCathelicidinsDNAInterferon-betaInterferon Type ILigandsTLR9 protein, humanToll-Like Receptor 9

Identifiers

PMID21850017
PMCPMC3220926
OpenAlexW2003164428

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.