Evidence map›Paper›PMID 25033445›Full record

ArticlePLoS pathogens2014

Syk signaling in dendritic cells orchestrates innate resistance to systemic fungal infection.

Paul G Whitney, Eva Bär, Fabiola Osorio, Neil C Rogers, Barbara U Schraml, Safia Deddouche, Salomé LeibundGut-Landmann, Caetano Reis e Sousa

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 58 papers.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed
4.4field-weighted citation impact, top 5% 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

58 citing papers in PubMed, 88 citations in OpenAlex.

  1. Article
  2. Article
  3. Isolation of Mouse Neutrophils.Current protocols · 2023
    Article
  4. Article
  5. Review
  6. Review
  7. Molecular association ofFrontiers in cellular and infection microbiology · 2023
    Review
  8. Review
  9. Review
  10. GM-CSFCell reports · 2022
    Article
  11. Article
  12. Review
  13. Article
  14. Review
  15. CD137 Signaling Is Critical in Fungal Clearance during SystemicJournal of fungi (Basel, Switzerland) · 2021
    Article
  16. Review
  17. Renal CD169Life science alliance · 2021
    Article
  18. The Interactions BetweenFrontiers in microbiology · 2021
    Review
  19. Immune Intervention in Sepsis.Frontiers in pharmacology · 2021
    Review
  20. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 3 institutions in 2 countries.

Paul G WhitneyImmunobiology Laboratory, Cancer Research UK, London Research Institute, Lincoln's Inn Fields Laboratories, London, United Kingdom.
Eva BärInstitute of Microbiology, ETH Zurich, Zürich, Switzerland.
Fabiola OsorioImmunobiology Laboratory, Cancer Research UK, London Research Institute, Lincoln's Inn Fields Laboratories, London, United Kingdom.
Neil C RogersImmunobiology Laboratory, Cancer Research UK, London Research Institute, Lincoln's Inn Fields Laboratories, London, United Kingdom.
Barbara U SchramlImmunobiology Laboratory, Cancer Research UK, London Research Institute, Lincoln's Inn Fields Laboratories, London, United Kingdom.
Safia DeddoucheImmunobiology Laboratory, Cancer Research UK, London Research Institute, Lincoln's Inn Fields Laboratories, London, United Kingdom.
Salomé LeibundGut-LandmannInstitute of Microbiology, ETH Zurich, Zürich, Switzerland.
Caetano Reis e SousaImmunobiology Laboratory, Cancer Research UK, London Research Institute, Lincoln's Inn Fields Laboratories, London, United Kingdom.
Cancer Research UK · GBThe Honourable Society of Lincoln's Inn · GBETH Zurich · CH

Funding

Cancer Research UK 15689Swiss National Science Foundation 123342
6 · The paper itself

Abstract

Host protection from fungal infection is thought to ensue in part from the activity of Syk-coupled C-type lectin receptors and MyD88-coupled toll-like receptors in myeloid cells, including neutrophils, macrophages and dendritic cells (DCs). Given the multitude of cell types and receptors involved, elimination of a single pathway for fungal recognition in a cell type such as DCs, primarily known for their ability to prime T cell responses, would be expected to have little effect on innate resistance to fungal infection. Here we report that this is surprisingly not the case and that selective loss of Syk but not MyD88 in DCs abrogates innate resistance to acute systemic Candida albicans infection in mice. We show that Syk expression by DCs is necessary for IL-23p19 production in response to C. albicans, which is essential to transiently induce GM-CSF secretion by NK cells that are recruited to the site of fungal replication. NK cell-derived-GM-CSF in turn sustains the anti-microbial activity of neutrophils, the main fungicidal effectors. Thus, the activity of a single kinase in a single myeloid cell type orchestrates a complex series of molecular and cellular events that underlies innate resistance to fungal sepsis.

Indexed as

Immunity, InnateAnimalsCandida albicansCandidiasisDendritic CellsInterleukin-23 Subunit p19Intracellular Signaling Peptides and ProteinsMiceMice, KnockoutMyeloid Differentiation Factor 88Protein-Tyrosine KinasesSyk KinaseIl23a protein, mouseInterleukin-23 Subunit p19Intracellular Signaling Peptides and ProteinsMyd88 protein, mouseMyeloid Differentiation Factor 88Protein-Tyrosine KinasesSyk KinaseSyk protein, mouse

Identifiers

PMID25033445
PMCPMC4102599
OpenAlexW2037320446

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.