Evidence map›Paper›PMID 29507358›Full record

ArticleScientific reports2018

Cathelicidin promotes inflammation by enabling binding of self-RNA to cell surface scavenger receptors.

Toshiya Takahashi, Nikhil Nitin Kulkarni, Ernest Y Lee, Ling-Juan Zhang, Gerard C L Wong, Richard L Gallo

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed
6.1field-weighted citation impact, top 3% 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

54 citing papers in PubMed, 83 citations in OpenAlex.

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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

6 authors at 2 institutions in 1 country.

Toshiya TakahashiDepartment of Dermatology, University of California, San Diego, La Jolla, CA, 92037, United States.
Nikhil Nitin KulkarniDepartment of Dermatology, University of California, San Diego, La Jolla, CA, 92037, United States.
Ernest Y LeeDepartment of Bioengineering, University of California, Los Angeles, Los Angeles, CA, 90095, United States.ORCID 0000-0001-5144-2552
Ling-Juan ZhangDepartment of Dermatology, University of California, San Diego, La Jolla, CA, 92037, United States.
Gerard C L WongDepartment of Bioengineering, University of California, Los Angeles, Los Angeles, CA, 90095, United States.
Richard L GalloDepartment of Dermatology, University of California, San Diego, La Jolla, CA, 92037, United States. rgallo@ucsd.edu.ORCID 0000-0002-1401-7861
University of California San Diego · USUniversity of California, Los Angeles · US

Funding

UCLA-Caltech Medical Scientist Training ProgramT32GM008042 · NIGMS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI AJIJOLA, OLUJIMI A, DAWSON, DAVID WAYNE · 1985 to 2023
$29.9M
Cathelicidins in Skin ImmunityR01AI052453 · NIAID · VETERANS MEDICAL RESEARCH FDN/SAN DIEGO · PI GALLO, RICHARD L, NIZET, VICTOR · 2002 to 2017
$5.3M
Systems in Integrative BiologyT32GM008185 · NIGMS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI CHOU, TOM · 1987 to 2022
$4.6M
Proteolysis and Skin AntimicrobialsR01AR052728 · NIAMS · VETERANS MEDICAL RESEARCH FDN/SAN DIEGO · PI GALLO, RICHARD L · 2006 to 2015
$3.3M
Skin Microbiome in epidermal immune defenseR01AI083358 · NIAID · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI GALLO, RICHARD L · 2010 to 2014
$1.9M
Dermatology Scientist Training ProgramT32AR071307 · NIAMS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI MODLIN, ROBERT L · 2017 to 2021
$1.1M
Glyco-therapeutics for Treating Persistent S. aureus Infections of Skin and Soft TissueR21AI122212 · NIAID · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI KASKO, ANDREA MARIE, WONG, GERARD C · 2016 to 2017
$399k
NIAID NIH HHS R01 AI052453NIAID NIH HHS R01 AI083358NIAID NIH HHS R21 AI122212NIAMS NIH HHS R01 AR052728NIAMS NIH HHS T32 AR071307NIGMS NIH HHS T32 GM008042NIGMS NIH HHS T32 GM008185
6 · The paper itself

Abstract

Under homeostatic conditions the release of self-RNA from dying cells does not promote inflammation. However, following injury or inflammatory skin diseases such as psoriasis and rosacea, expression of the cathelicidin antimicrobial peptide LL37 breaks tolerance to self-nucleic acids and triggers inflammation. Here we report that LL37 enables keratinocytes and macrophages to recognize self-non-coding U1 RNA by facilitating binding to cell surface scavenger receptors that enable recognition by nucleic acid pattern recognition receptors within the cell. The interaction of LL37 with scavenger receptors was confirmed in human psoriatic skin, and the ability of LL37 to stimulate expression of interleukin-6 and interferon-β1 was dependent on a 3-way binding interaction with scavenger receptors and subsequent clathrin-mediated endocytosis. These results demonstrate that the inflammatory activity of LL37 is mediated by a cell-surface-dependent interaction and provides important new insight into mechanisms that drive auto-inflammatory responses in the skin.

Indexed as

Antimicrobial Cationic PeptidesBinding SitesCathelicidinsCells, CulturedHumansInflammationReceptors, ScavengerRNAAntimicrobial Cationic PeptidesCathelicidinsReceptors, ScavengerRNA

Identifiers

PMID29507358
PMCPMC5838106
OpenAlexW2805903031

What OpenQuestion holds

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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 OpenQuestion graph.