Evidence map›Paper›PMID 34302006›Full record

ArticleScientific reports2021

Ly6G deficiency alters the dynamics of neutrophil recruitment and pathogen capture during Leishmania major skin infection.

Corinna L Kleinholz, Monika Riek-Burchardt, Elena A Seiß, Jonas Amore, Patricia Gintschel, Lars Philipsen, Philippe Bousso, Borna Relja, Burkhart Schraven, Juliane Handschuh and 2 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
4.1field-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

23 citing papers in PubMed, 38 citations in OpenAlex.

  1. Lymphocyte Antigen 6G Mediates Vagotomy-Associated Reduction in Body Weight.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
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  15. Type I IFN signaling in the absence of IRGM1 promotesbioRxiv : the preprint server for biology · 2023
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  19. Dual wave of neutrophil recruitment determines the outcome ofFrontiers in cellular and infection microbiology · 2023
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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

12 authors at 3 institutions in 2 countries.

Corinna L KleinholzInstitute of Molecular and Clinical Immunology, Health Campus Immunology Infectiology and Inflammation (GC-I3), Otto-Von-Guericke-University, Leipziger Strasse 44, 39120, Magdeburg, Germany.
Monika Riek-BurchardtInstitute of Molecular and Clinical Immunology, Health Campus Immunology Infectiology and Inflammation (GC-I3), Otto-Von-Guericke-University, Leipziger Strasse 44, 39120, Magdeburg, Germany.
Elena A SeißInstitute of Molecular and Clinical Immunology, Health Campus Immunology Infectiology and Inflammation (GC-I3), Otto-Von-Guericke-University, Leipziger Strasse 44, 39120, Magdeburg, Germany.
Jonas AmoreInstitute of Molecular and Clinical Immunology, Health Campus Immunology Infectiology and Inflammation (GC-I3), Otto-Von-Guericke-University, Leipziger Strasse 44, 39120, Magdeburg, Germany.
Patricia GintschelInstitute of Molecular and Clinical Immunology, Health Campus Immunology Infectiology and Inflammation (GC-I3), Otto-Von-Guericke-University, Leipziger Strasse 44, 39120, Magdeburg, Germany.
Lars PhilipsenInstitute of Molecular and Clinical Immunology, Health Campus Immunology Infectiology and Inflammation (GC-I3), Otto-Von-Guericke-University, Leipziger Strasse 44, 39120, Magdeburg, Germany.
Philippe BoussoDepartment of Immunology, Dynamics of Immune Responses, Institut Pasteur, 25 Rue du Docteur Roux, 75015, Paris, France.
Borna ReljaUniversity Clinic for Radiology and Nuclear Medicine, Otto-Von-Guericke-University, Leipziger Strasse 44, 39120, Magdeburg, Germany.
Burkhart SchravenInstitute of Molecular and Clinical Immunology, Health Campus Immunology Infectiology and Inflammation (GC-I3), Otto-Von-Guericke-University, Leipziger Strasse 44, 39120, Magdeburg, Germany.
Juliane HandschuhInstitute of Molecular and Clinical Immunology, Health Campus Immunology Infectiology and Inflammation (GC-I3), Otto-Von-Guericke-University, Leipziger Strasse 44, 39120, Magdeburg, Germany.
Juliane MohrInstitute of Molecular and Clinical Immunology, Health Campus Immunology Infectiology and Inflammation (GC-I3), Otto-Von-Guericke-University, Leipziger Strasse 44, 39120, Magdeburg, Germany. juliane2.mohr@med.ovgu.de.
Andreas J MüllerInstitute of Molecular and Clinical Immunology, Health Campus Immunology Infectiology and Inflammation (GC-I3), Otto-Von-Guericke-University, Leipziger Strasse 44, 39120, Magdeburg, Germany. andreas.mueller@med.ovgu.de.
Otto-von-Guericke University Magdeburg · DEHelmholtz Centre for Infection Research · DEInstitut Pasteur · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neutrophils represent one of the first immune cell types recruited to sites of infection, where they can control pathogens by phagocytosis and cytotoxic mechanisms. Intracellular pathogens such as Leishmania major can hijack neutrophils to establish an efficient infection. However the dynamic interactions of neutrophils with the pathogen and other cells at the site of the infection are incompletely understood. Here, we have investigated the role of Ly6G, a homolog of the human CD177 protein, which has been shown to interact with cell adhesion molecules, and serves as a bona fide marker for neutrophils in mice. We show that Ly6G deficiency decreases the initial infection rate of neutrophils recruited to the site of infection. Although the uptake of L. major by subsequently recruited monocytes was tightly linked with the concomitant uptake of neutrophil material, this process was not altered by Ly6G deficiency of the neutrophils. Instead, we observed by intravital 2-photon microscopy that Ly6G-deficient neutrophils entered the site of infection with delayed initial recruitment kinetics. Thus, we conclude that by promoting neutrophils' ability to efficiently enter the site of infection, Ly6G contributes to the early engagement of intracellular pathogens by the immune system.

Indexed as

AnimalsAntigens, LyDisease Models, AnimalHumansLeishmania majorLeishmaniasis, CutaneousMiceMonocytesNeutrophil InfiltrationNeutrophilsPhagocytosisSkinAntigens, LyLy6G antigen, mouse

Identifiers

PMID34302006
PMCPMC8302578
OpenAlexW3186050572

What OpenQuestion holds

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Registered trials

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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.