Evidence map›Paper›PMID 39622833›Full record

ArticleNature communications2024

Lack of TYK2 signaling enhances host resistance to Candida albicans skin infection.

Sara Miranda, Caroline Lassnig, Kristina Schmidhofer, Hrönn Kjartansdottir, Claus Vogl, Simone Tangermann, Irina Tsymala, Verena Babl, Mathias Müller, Karl Kuchler and 1 more

Abstract read
In one paragraph

Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. A new heterozygous TYK2 gene mutation: Case report and review of the literature.International journal of immunopathology and pharmacology
    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

11 authors.

Sara MirandaCentre of Biological Sciences, University of Veterinary Medicine Vienna, Vienna, Austria.
Caroline LassnigCentre of Biological Sciences, University of Veterinary Medicine Vienna, Vienna, Austria.
Kristina SchmidhoferCentre of Biological Sciences, University of Veterinary Medicine Vienna, Vienna, Austria.
Hrönn KjartansdottirCentre of Biological Sciences, University of Veterinary Medicine Vienna, Vienna, Austria.ORCID 0000-0002-2322-3050
Claus VoglCentre of Biological Sciences, University of Veterinary Medicine Vienna, Vienna, Austria.ORCID 0000-0002-3996-7863
Simone TangermannCentre of Pathobiology, University of Veterinary Medicine Vienna, Vienna, Austria.
Irina TsymalaMax Perutz Labs, Vienna Biocenter Campus (VBC), Vienna, Austria.
Verena BablCentre of Biological Sciences, University of Veterinary Medicine Vienna, Vienna, Austria.
Mathias MüllerCentre of Biological Sciences, University of Veterinary Medicine Vienna, Vienna, Austria.ORCID 0000-0002-7879-3552
Karl KuchlerMax Perutz Labs, Vienna Biocenter Campus (VBC), Vienna, Austria.ORCID 0000-0003-2719-5955
Birgit StroblCentre of Biological Sciences, University of Veterinary Medicine Vienna, Vienna, Austria. birgit.strobl@vetmeduni.ac.at.ORCID 0000-0001-5716-3212

Funding

Austrian Science Fund (Fonds zur Förderung der Wissenschaftlichen Forschung) ChromFunVirAustrian Science Fund (Fonds zur Förderung der Wissenschaftlichen Forschung) DOC32-B28Austrian Science Fund (Fonds zur Förderung der Wissenschaftlichen Forschung) P-32582-B08Austrian Science Fund (Fonds zur Förderung der Wissenschaftlichen Forschung) P34286-BAustrian Science Fund (Fonds zur Förderung der Wissenschaftlichen Forschung) SFB-F6101
6 · The paper itself

Abstract

Candida albicans is the most common human fungal pathogen, causing diseases ranging from local to life-threating systemic infections. Tyrosine kinase 2 (TYK2), a crucial mediator in several cytokine signaling pathways, has been associated with protective functions in various microbial infections. However, its specific contribution in the immune response to fungal infections has remained elusive. In this study, we show that mice lacking TYK2 or its enzymatic activity exhibit enhanced resistance to C. albicans skin infections, limiting fungal spread and accelerating wound healing. Impaired TYK2-signaling prompted the formation of a distinctive layer of necrotic neutrophils around the fungal pathogens. Transcriptomic analysis revealed TYK2's pivotal role in regulating interferon-inducible genes in neutrophils, thereby impacting their antifungal capacity during infection. Furthermore, we show that TYK2-dependent interferon-gamma (IFNγ) production contributes to fungal dissemination from the skin to the kidneys. Our study uncovers a hitherto unrecognized detrimental role of TYK2 in cutaneous C. albicans infections.

Indexed as

Candida albicansInterferon-gammaMice, Inbred C57BLMice, KnockoutNeutrophilsSignal TransductionTYK2 KinaseAnimalsCandidiasisCandidiasis, CutaneousFemaleMaleMiceSkinWound HealingInterferon-gammaTYK2 KinaseTyk2 protein, mouse

Identifiers

PMID39622833
PMCPMC11612186

What Socratic 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 Socratic graph.