Evidence map›Paper›PMID 31913271›Full record

ArticleNature communications2020

Neutrophil extracellular trap-associated RNA and LL37 enable self-amplifying inflammation in psoriasis.

Franziska Herster, Zsofia Bittner, Nathan K Archer, Sabine Dickhöfer, David Eisel, Tatjana Eigenbrod, Thomas Knorpp, Nicole Schneiderhan-Marra, Markus W Löffler, Hubert Kalbacher and 9 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 152 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
152citing papers in PubMed, 1 pooled it
11.4field-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

152 citing papers in PubMed, 1 synthesis or guideline pooled it, 265 citations in OpenAlex.

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  17. The Ly6gCancer communications (London, England) · 2026
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92 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

19 authors at 8 institutions in 3 countries.

Franziska HersterDepartment of Immunology, University of Tübingen, Auf der Morgenstelle 15, 72076, Tübingen, Germany.ORCID http://orcid.org/0000-0003-1512-7306
Zsofia BittnerDepartment of Immunology, University of Tübingen, Auf der Morgenstelle 15, 72076, Tübingen, Germany.
Nathan K ArcherDepartment of Dermatology, Johns Hopkins University School of Medicine, Baltimore, MD, 21231, USA.
Sabine DickhöferDepartment of Immunology, University of Tübingen, Auf der Morgenstelle 15, 72076, Tübingen, Germany.
David EiselDepartment of Immunology, University of Tübingen, Auf der Morgenstelle 15, 72076, Tübingen, Germany.
Tatjana EigenbrodDepartment of Infectious Diseases, Medical Microbiology and Hygiene, University Hospital Heidelberg, Im Neuenheimer Feld 324, 69120, Heidelberg, Germany.
Thomas KnorppNMI Natural and Medical Sciences Institute at the University of Tübingen, Markwiesenstr. 55, 72770, Reutlingen, Germany.
Nicole Schneiderhan-MarraNMI Natural and Medical Sciences Institute at the University of Tübingen, Markwiesenstr. 55, 72770, Reutlingen, Germany.ORCID http://orcid.org/0000-0001-6785-181X
Markus W LöfflerDepartment of Immunology, University of Tübingen, Auf der Morgenstelle 15, 72076, Tübingen, Germany.ORCID http://orcid.org/0000-0003-2513-1317
Hubert KalbacherInterfaculty Institute of Biochemistry, University of Tübingen, Hoppe-Seyler-Str. 4, 72076, Tübingen, Germany.ORCID http://orcid.org/0000-0002-7862-277X
Tim VierbuchenResearch Group Innate Immunity, Research Center Borstel, Leibniz Lung Center, Airway Research Center North (ARCN), Deutsches Zentrum für Lungenforschung (DZL), Parkallee 22, 23845, Borstel, Germany.ORCID http://orcid.org/0000-0003-3110-4155
Holger HeineResearch Group Innate Immunity, Research Center Borstel, Leibniz Lung Center, Airway Research Center North (ARCN), Deutsches Zentrum für Lungenforschung (DZL), Parkallee 22, 23845, Borstel, Germany.ORCID http://orcid.org/0000-0001-8128-5068
Lloyd S MillerDepartment of Dermatology, Johns Hopkins University School of Medicine, Baltimore, MD, 21231, USA.
Dominik HartlUniversity Children's Hospital and Interdisciplinary Center for Infectious Diseases, University of Tübingen, Hoppe-Seyler-Str. 1, 72076, Tübingen, Germany.
Lukas FreundDepartment of Dermatology, University Hospital Heidelberg, Im Neuenheimer Feld 440, 69120, Heidelberg, Germany.
Knut SchäkelDepartment of Dermatology, University Hospital Heidelberg, Im Neuenheimer Feld 440, 69120, Heidelberg, Germany.ORCID http://orcid.org/0000-0001-6344-7799
Martin HeisterDepartment of Dermatology, University Hospital Tübingen, Liebermeisterstr. 25, 72076, Tübingen, Germany.
Kamran GhoreschiDepartment of Dermatology, University Hospital Tübingen, Liebermeisterstr. 25, 72076, Tübingen, Germany.
Alexander N R WeberDepartment of Immunology, University of Tübingen, Auf der Morgenstelle 15, 72076, Tübingen, Germany. alexander.weber@uni-tuebingen.de.ORCID http://orcid.org/0000-0002-8627-7056
University of Tübingen · DEHeidelberg University · DEUniversity Children's Hospital Tübingen · DEJohns Hopkins University · USNatural and Medical Sciences Institute · DEResearch Center Borstel - Leibniz Lung Center · DEBioNTech (Germany) · DENovartis (Switzerland) · CH

Funding

IL-36 responses in Staphylococcus aureus driven skin inflammationR01AR073665 · NIAMS · JOHNS HOPKINS UNIVERSITY · PI ARCHER, NATHAN K. · 2018 to 2022
$1.8M
STAT3-mediated immunity to Staphylococcus aureus in skinR01AR069502 · NIAMS · JOHNS HOPKINS UNIVERSITY · PI ARCHER, NATHAN K. · 2016 to 2020
$1.8M
NIAMS NIH HHS R01 AR069502NIAMS NIH HHS R01 AR073665
6 · The paper itself

Abstract

Psoriasis is an inflammatory skin disease with strong neutrophil (PMN) infiltration and high levels of the antimicrobial peptide, LL37. LL37 in complex with DNA and RNA is thought to initiate disease exacerbation via plasmacytoid dendritic cells. However, the source of nucleic acids supposed to start this initial inflammatory event remains unknown. We show here that primary murine and human PMNs mount a fulminant and self-propagating neutrophil extracellular trap (NET) and cytokine response, but independently of the canonical NET component, DNA. Unexpectedly, RNA, which is abundant in NETs and psoriatic but not healthy skin, in complex with LL37 triggered TLR8/TLR13-mediated cytokine and NET release by PMNs in vitro and in vivo. Transfer of NETs to naive human PMNs prompts additional NET release, promoting further inflammation. Our study thus uncovers a self-propagating vicious cycle contributing to chronic inflammation in psoriasis, and NET-associated RNA (naRNA) as a physiologically relevant NET component.

Indexed as

AdultAnimalsAntimicrobial Cationic PeptidesCathelicidinsCytokinesExtracellular TrapsFemaleHumansMaleMiceMice, Inbred C57BLMiddle AgedNeutrophil InfiltrationNeutrophilsPsoriasisRNAAntimicrobial Cationic PeptidesCathelicidinsCytokinesRNAToll-Like Receptor 8

Identifiers

PMID31913271
PMCPMC6949246
OpenAlexW2999043338

What OpenQuestion holds

Textmetadata
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.