Evidence map›Paper›PMID 31887131›Full record

ArticlePLoS pathogens2019

IL-23 supports host defense against systemic Candida albicans infection by ensuring myeloid cell survival.

Selim Nur, Florian Sparber, Christina Lemberg, Eva Guiducci, Tiziano A Schweizer, Pascale Zwicky, Burkhard Becher, Salomé LeibundGut-Landmann

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.4field-weighted citation impact, top 10% 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

24 citing papers in PubMed, 40 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. ANKRD22 promotes resolution of psoriasiform skin inflammation by antagonizing NIK-mediated IL-23 production.Molecular therapy : the journal of the American Society of Gene Therapy · 2024
    Article
  6. Article
  7. Review
  8. Article
  9. Genetic Susceptibility to Fungal Infections.Advanced biomedical research · 2023
    Review
  10. Review
  11. Article
  12. Article
  13. A Fun-Guide to Innate Immune Responses to Fungal Infections.Journal of fungi (Basel, Switzerland) · 2022
    Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Review
  19. Article
  20. 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

8 authors at 1 institution in 1 country.

Selim NurSection of Immunology, Vetsuisse Faculty, University of Zürich, Zürich, Switzerland.
Florian SparberSection of Immunology, Vetsuisse Faculty, University of Zürich, Zürich, Switzerland.ORCID 0000-0003-4224-724X
Christina LembergSection of Immunology, Vetsuisse Faculty, University of Zürich, Zürich, Switzerland.ORCID 0000-0003-4327-3394
Eva GuiducciSection of Immunology, Vetsuisse Faculty, University of Zürich, Zürich, Switzerland.ORCID 0000-0002-5602-690X
Tiziano A SchweizerSection of Immunology, Vetsuisse Faculty, University of Zürich, Zürich, Switzerland.
Pascale ZwickyInstitute of Experimental Immunology, University of Zürich, Zürich, Switzerland.ORCID 0000-0003-0419-2153
Burkhard BecherInstitute of Experimental Immunology, University of Zürich, Zürich, Switzerland.ORCID 0000-0002-1541-7867
Salomé LeibundGut-LandmannSection of Immunology, Vetsuisse Faculty, University of Zürich, Zürich, Switzerland.ORCID 0000-0002-5724-4837
University of Zurich · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The opportunistic fungal pathogen Candida albicans can cause invasive infections in susceptible hosts and the innate immune system, in particular myeloid cell-mediated immunity, is critical for rapid immune protection and host survival during systemic candidiasis. Using a mouse model of the human disease, we identified a novel role of IL-23 in antifungal defense. IL-23-deficient mice are highly susceptible to systemic infection with C. albicans. We found that this results from a drastic reduction in all subsets of myeloid cells in the infected kidney, which in turn leads to rapid fungal overgrowth and renal tissue injury. The loss in myeloid cells is not due to a defect in emergency myelopoiesis or the recruitment of newly generated cells to the site of infection but, rather, is a consequence of impaired survival of myeloid cells at the site of infection. In fact, the absence of a functional IL-23 pathway causes massive myeloid cell apoptosis upon C. albicans infection. Importantly, IL-23 protects myeloid cells from apoptosis independently of the IL-23-IL-17 immune axis and independently of lymphocytes and innate lymphoid cells. Instead, our results suggest that IL-23 acts in a partially autocrine but not cell-intrinsic manner within the myeloid compartment to promote host protection from systemic candidiasis. Collectively, our data highlight an unprecedented and non-canonical role of IL-23 in securing survival of myeloid cells, which is key for maintaining sufficient numbers of cells at the site of infection to ensure efficient host protection.

Indexed as

AnimalsCandida albicansCell SurvivalHost-Pathogen InteractionsImmunity, InnateInterleukin-17Interleukin-23LymphocytesMice, Inbred C57BLMyeloid CellsMyeloid Progenitor CellsInterleukin-17Interleukin-23

Identifiers

PMID31887131
PMCPMC6957211
OpenAlexW2997592064

What OpenQuestion holds

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LicenceCC BY
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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.