Evidence map›Paper›PMID 38889192›Full record

ArticlePLoS pathogens2024

CD56-mediated activation of human natural killer cells is triggered by Aspergillus fumigatus galactosaminogalactan.

Linda Heilig, Fariha Natasha, Nora Trinks, Vishukumar Aimanianda, Sarah Sze Wah Wong, Thierry Fontaine, Ulrich Terpitz, Lea Strobel, François Le Mauff, Donald C Sheppard and 10 more

Abstract read
In one paragraph

Article in PLoS pathogens, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
–field-weighted citation impact
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

9 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. Interplay of Cytokines and Chemokines in Aspergillosis.Journal of fungi (Basel, Switzerland) · 2024
    Review
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

20 authors.

Linda HeiligDepartment of Internal Medicine II, University Hospital Wuerzburg, Wuerzburg, Germany.ORCID 0009-0004-2255-5178
Fariha NatashaDepartment of Biotechnology & Biophysics Biocenter, University of Wuerzburg, Wuerzburg, Germany.
Nora TrinksDepartment of Biotechnology & Biophysics Biocenter, University of Wuerzburg, Wuerzburg, Germany.
Vishukumar AimaniandaDepartment of Mycology, Immunobiology of Aspergillus, Institut Pasteur, Paris, France.
Sarah Sze Wah WongDepartment of Mycology, Immunobiology of Aspergillus, Institut Pasteur, Paris, France.
Thierry FontaineInstitut Pasteur, Université Paris Cité, INRAE, USC2019, Fungal Biology and Pathogenicity laboratory, Paris, France.
Ulrich TerpitzDepartment of Biotechnology & Biophysics Biocenter, University of Wuerzburg, Wuerzburg, Germany.
Lea StrobelDepartment of Internal Medicine II, University Hospital Wuerzburg, Wuerzburg, Germany.
François Le MauffInfectious Disease in Global Health Program, McGill University Health Centre, Montreal, Canada.
Donald C SheppardInfectious Disease in Global Health Program, McGill University Health Centre, Montreal, Canada.
Sascha SchäubleDepartment of Microbiome Dynamics, Leibniz Institute for Natural Product Research and Infection Biology-Hans Knöll Institute (HKI), Jena, Germany.
Oliver KurzaiInstitute for Hygiene und Microbiology, University of Wuerzburg, Wuerzburg, Germany.
Kerstin HünnigerInstitute for Hygiene und Microbiology, University of Wuerzburg, Wuerzburg, Germany.
Esther WeissDepartment of Internal Medicine II, University Hospital Wuerzburg, Wuerzburg, Germany.
Mario VargasProgram in Molecular Medicine, Research Institute, The Hospital for Sick Children, Toronto, Canada.
P Lynne HowellProgram in Molecular Medicine, Research Institute, The Hospital for Sick Children, Toronto, Canada.
Gianni PanagiotouDepartment of Microbiome Dynamics, Leibniz Institute for Natural Product Research and Infection Biology-Hans Knöll Institute (HKI), Jena, Germany.
Sebastian WursterDepartment of Infectious Diseases, Infection Control and Employee Health, The University of Texas MD Anderson Cancer Center, Houston, Texas, United States of America.
Hermann EinseleDepartment of Internal Medicine II, University Hospital Wuerzburg, Wuerzburg, Germany.
Juergen LoefflerDepartment of Internal Medicine II, University Hospital Wuerzburg, Wuerzburg, Germany.ORCID 0000-0001-6619-1100

Funding

Agence Nationale de la Recherche (ANR) ANR-21-CE17-0032-01Deutsche Forschungsgemeinschaft (DFG) 210879364
6 · The paper itself

Abstract

Invasive aspergillosis causes significant morbidity and mortality in immunocompromised patients. Natural killer (NK) cells are pivotal for antifungal defense. Thus far, CD56 is the only known pathogen recognition receptor on NK cells triggering potent antifungal activity against Aspergillus fumigatus. However, the underlying cellular mechanisms and the fungal ligand of CD56 have remained unknown. Using purified cell wall components, biochemical treatments, and ger mutants with altered cell wall composition, we herein found that CD56 interacts with the A. fumigatus cell wall carbohydrate galactosaminogalactan (GAG). This interaction induced NK-cell activation, degranulation, and secretion of immune-enhancing chemokines and cytotoxic effectors. Supernatants from GAG-stimulated NK cells elicited antifungal activity and enhanced antifungal effector responses of polymorphonuclear cells. In conclusion, we identified A. fumigatus GAG as a ligand of CD56 on human primary NK cells, stimulating potent antifungal effector responses and activating other immune cells.

Indexed as

AspergillosisAspergillus fumigatusCD56 AntigenKiller Cells, NaturalCell WallHumansLymphocyte ActivationPolysaccharidesCD56 AntigengalactosaminogalactanNCAM1 protein, humanPolysaccharides

Identifiers

PMID38889192
PMCPMC11216564

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.