Evidence map›Paper›PMID 34349124›Full record

ArticleNature communications2021

NK cells in hypoxic skin mediate a trade-off between wound healing and antibacterial defence.

Michal Sobecki, Ewelina Krzywinska, Shunmugam Nagarajan, Annette Audigé, Khanh Huỳnh, Julian Zacharjasz, Julien Debbache, Yann Kerdiles, Dagmar Gotthardt, Norihiko Takeda and 4 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
3.4field-weighted citation impact, top 6% 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

46 citing papers in PubMed, 62 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

14 authors at 5 institutions in 5 countries.

Michal Sobecki *University of Zurich, Institute of Anatomy, Zurich, Switzerland.ORCID 0000-0002-8177-0327
Ewelina Krzywinska *University of Zurich, Institute of Anatomy, Zurich, Switzerland.ORCID 0000-0002-4311-2972
Shunmugam NagarajanUniversity of Zurich, Institute of Anatomy, Zurich, Switzerland.
Annette AudigéUniversity of Zurich, Institute of Anatomy, Zurich, Switzerland.
Khanh HuỳnhUniversity of Zurich, Institute of Anatomy, Zurich, Switzerland.
Julian ZacharjaszUniversity of Zurich, Institute of Anatomy, Zurich, Switzerland.ORCID 0000-0003-2091-7070
Julien DebbacheUniversity of Zurich, Institute of Anatomy, Zurich, Switzerland.
Yann KerdilesCentre d'Immunologie de Marseille-Luminy, Aix Marseille Université UM2, Inserm, U1104, CNRS UMR7280, Marseille, France.ORCID 0000-0002-8605-1073
Dagmar GotthardtInstitute of Pharmacology and Toxicology, University of Veterinary Medicine, Vienna, Austria.ORCID 0000-0002-8416-1236
Norihiko TakedaDivision of Cardiology and Metabolism, Center for Molecular Medicine, Jichi Medical University, 3311-1 Yakushiji, Tochigi, Japan.
Joachim FandreyInstitut für Physiologie, Universitätsklinikum Essen, Universität Duisburg-Essen, Essen, Germany.ORCID 0000-0001-9585-0531
Lukas SommerUniversity of Zurich, Institute of Anatomy, Zurich, Switzerland.ORCID 0000-0002-1143-7908
Veronika SexlInstitute of Pharmacology and Toxicology, University of Veterinary Medicine, Vienna, Austria.
Christian StockmannUniversity of Zurich, Institute of Anatomy, Zurich, Switzerland. christian.stockmann@anatomy.uzh.ch.ORCID 0000-0002-9726-6838
University of Zurich · CHUniversity of Veterinary Medicine Vienna · ATCentre National de la Recherche Scientifique · FREssen University Hospital · DEJichi Medical University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

During skin injury, immune response and repair mechanisms have to be coordinated for rapid skin regeneration and the prevention of microbial infections. Natural Killer (NK) cells infiltrate hypoxic skin lesions and Hypoxia-inducible transcription factors (HIFs) mediate adaptation to low oxygen. We demonstrate that mice lacking the Hypoxia-inducible factor (HIF)-1α isoform in NK cells show impaired release of the cytokines Interferon (IFN)-γ and Granulocyte Macrophage - Colony Stimulating Factor (GM-CSF) as part of a blunted immune response. This accelerates skin angiogenesis and wound healing. Despite rapid wound closure, bactericidal activity and the ability to restrict systemic bacterial infection are impaired. Conversely, forced activation of the HIF pathway supports cytokine release and NK cell-mediated antibacterial defence including direct killing of bacteria by NK cells despite delayed wound closure. Our results identify, HIF-1α in NK cells as a nexus that balances antimicrobial defence versus global repair in the skin.

Indexed as

Wound HealingAnimalsCell HypoxiaCytokinesHypoxiaHypoxia-Inducible Factor 1, alpha SubunitKiller Cells, NaturalMiceNeovascularization, PhysiologicSkinSkin Diseases, BacterialCytokinesHif1a protein, mouseHypoxia-Inducible Factor 1, alpha Subunit

Identifiers

PMID34349124
PMCPMC8338923
OpenAlexW3189787010

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.