Evidence map›Paper›PMID 25129145›Full record

ArticleNature genetics2014

Jagunal homolog 1 is a critical regulator of neutrophil function in fungal host defense.

Gerald Wirnsberger, Florian Zwolanek, Johannes Stadlmann, Luigi Tortola, Shang Wan Liu, Thomas Perlot, Päivi Järvinen, Gerhard Dürnberger, Ivona Kozieradzki, Renu Sarao and 7 more

Open access · greenAbstract read
In one paragraph

Article in Nature genetics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
3.6field-weighted citation impact, top 7% 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

34 citing papers in PubMed, 64 citations in OpenAlex.

  1. Article
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  4. Review
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  7. Review
  8. Akt-2 Is a Potential Therapeutic Target for Disseminated Candidiasis.Journal of immunology (Baltimore, Md. : 1950) · 2022
    Article
  9. Article
  10. Article
  11. The δ subunit of FNature communications · 2021
    Article
  12. HECT E3 Ubiquitin Ligase Nedd4 Is Required for Antifungal Innate Immunity.Journal of immunology (Baltimore, Md. : 1950) · 2021
    Article
  13. Identification ofPathogens (Basel, Switzerland) · 2021
    Article
  14. Article
  15. Immune Sensing ofJournal of fungi (Basel, Switzerland) · 2021
    Review
  16. Article
  17. Article
  18. Article
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  20. Article
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

17 authors at 6 institutions in 2 countries.

Gerald WirnsbergerInstitute of Molecular Biotechnology of the Austrian Academy of Sciences (IMBA), Vienna, Austria.
Florian ZwolanekDepartment of Medical Biochemistry, Max F. Perutz Laboratories, Medical University of Vienna, Vienna, Austria.
Johannes Stadlmann1] Institute of Molecular Biotechnology of the Austrian Academy of Sciences (IMBA), Vienna, Austria. [2] Institute for Molecular Pathology (IMP), Vienna, Austria.
Luigi TortolaInstitute of Molecular Biotechnology of the Austrian Academy of Sciences (IMBA), Vienna, Austria.
Shang Wan LiuInstitute of Molecular Biotechnology of the Austrian Academy of Sciences (IMBA), Vienna, Austria.
Thomas PerlotInstitute of Molecular Biotechnology of the Austrian Academy of Sciences (IMBA), Vienna, Austria.
Päivi JärvinenDepartment of Pediatrics, Dr. Von Hauner Children's Hospital, Ludwig Maximilians University, Munich, Germany.
Gerhard Dürnberger1] Institute of Molecular Biotechnology of the Austrian Academy of Sciences (IMBA), Vienna, Austria. [2] Institute for Molecular Pathology (IMP), Vienna, Austria.
Ivona KozieradzkiInstitute of Molecular Biotechnology of the Austrian Academy of Sciences (IMBA), Vienna, Austria.
Renu SaraoInstitute of Molecular Biotechnology of the Austrian Academy of Sciences (IMBA), Vienna, Austria.
Alba De MartinoCampus Science Support Facility (CSF), Vienna, Austria.
Kaan Boztug1] Research Center for Molecular Medicine of the Austrian Academy of Sciences (CeMM), Vienna, Austria. [2] Department of Pediatrics and Adolescent Medicine, Medical University of Vienna, Vienna, Austria.
Karl Mechtler1] Institute of Molecular Biotechnology of the Austrian Academy of Sciences (IMBA), Vienna, Austria. [2] Institute for Molecular Pathology (IMP), Vienna, Austria.
Karl KuchlerDepartment of Medical Biochemistry, Max F. Perutz Laboratories, Medical University of Vienna, Vienna, Austria.
Christoph KleinDepartment of Pediatrics, Dr. Von Hauner Children's Hospital, Ludwig Maximilians University, Munich, Germany.
Ulrich EllingInstitute of Molecular Biotechnology of the Austrian Academy of Sciences (IMBA), Vienna, Austria.
Josef M PenningerInstitute of Molecular Biotechnology of the Austrian Academy of Sciences (IMBA), Vienna, Austria.
Austrian Academy of Sciences · ATInstitute of Molecular Biotechnology · ATLudwig-Maximilians-Universität München · DEMedical University of Vienna · ATCeMM Research Center for Molecular Medicine · ATResearch Institute of Molecular Pathology · AT

Funding

Austrian Science Fund FWF P 24685Austrian Science Fund FWF P 25333Austrian Science Fund FWF TRP 308European Research Council 341036
6 · The paper itself

Abstract

Neutrophils are key innate immune effector cells that are essential to fighting bacterial and fungal pathogens. Here we report that mice carrying a hematopoietic lineage-specific deletion of Jagn1 (encoding Jagunal homolog 1) cannot mount an efficient neutrophil-dependent immune response to the human fungal pathogen Candida albicans. Global glycobiome analysis identified marked alterations in the glycosylation of proteins involved in cell adhesion and cytotoxicity in Jagn1-deficient neutrophils. Functional analysis confirmed marked defects in neutrophil migration in response to Candida albicans infection and impaired formation of cytotoxic granules, as well as defective myeloperoxidase release and killing of Candida albicans. Treatment with granulocyte/macrophage colony-stimulating factor (GM-CSF) protected mutant mice from increased weight loss and accelerated mortality after Candida albicans challenge. Notably, GM-CSF also restored the defective fungicidal activity of bone marrow cells from humans with JAGN1 mutations. These data directly identify Jagn1 (JAGN1 in humans) as a new regulator of neutrophil function in microbial pathogenesis and uncover a potential treatment option for humans.

Indexed as

AnimalsBone Marrow CellsCandida albicansCandidiasisGlycosylationGranulocyte-Macrophage Colony-Stimulating FactorHumansMaleMembrane ProteinsMiceNeutrophilsGranulocyte-Macrophage Colony-Stimulating FactorJAGN1 protein, humanMembrane Proteins

Identifiers

PMID25129145
PMCPMC6245568
OpenAlexW2057749456

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.