Evidence map›Paper›PMID 25474208›Full record

ArticlePLoS pathogens2014

The non-receptor tyrosine kinase Tec controls assembly and activity of the noncanonical caspase-8 inflammasome.

Florian Zwolanek, Michael Riedelberger, Valentina Stolz, Sabrina Jenull, Fabian Istel, Afitap Derya Köprülü, Wilfried Ellmeier, Karl Kuchler

Open 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. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

27 citing papers in PubMed, 42 citations in OpenAlex.

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  16. Modulating Host Signaling Pathways to Promote Resistance to Infection byFrontiers in cellular and infection microbiology · 2017
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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 2 institutions in 1 country.

Florian ZwolanekDepartment of Molecular Genetics, Medical University of Vienna, Max F. Perutz Laboratories, Vienna, Austria.
Michael RiedelbergerDepartment of Molecular Genetics, Medical University of Vienna, Max F. Perutz Laboratories, Vienna, Austria.
Valentina StolzDepartment of Molecular Genetics, Medical University of Vienna, Max F. Perutz Laboratories, Vienna, Austria.
Sabrina JenullDepartment of Molecular Genetics, Medical University of Vienna, Max F. Perutz Laboratories, Vienna, Austria.
Fabian IstelDepartment of Molecular Genetics, Medical University of Vienna, Max F. Perutz Laboratories, Vienna, Austria.
Afitap Derya KöprülüDivision of Immunobiology, Institute of Immunology, Center for Pathophysiology, Infectiology and Immunology, Medical University of Vienna, Vienna, Austria.
Wilfried EllmeierDivision of Immunobiology, Institute of Immunology, Center for Pathophysiology, Infectiology and Immunology, Medical University of Vienna, Vienna, Austria.
Karl KuchlerDepartment of Molecular Genetics, Medical University of Vienna, Max F. Perutz Laboratories, Vienna, Austria.
Medical University of Vienna · ATMax Perutz Labs · AT

Funding

Austrian Science Fund FWF P 25333
6 · The paper itself

Abstract

Tec family kinases are intracellular non-receptor tyrosine kinases implicated in numerous functions, including T cell and B cell regulation. However, a role in microbial pathogenesis has not been described. Here, we identified Tec kinase as a novel key mediator of the inflammatory immune response in macrophages invaded by the human fungal pathogen C. albicans. Tec is required for both activation and assembly of the noncanonical caspase-8, but not of the caspase-1 inflammasome, during infections with fungal but not bacterial pathogens, triggering the antifungal response through IL-1β. Furthermore, we identify dectin-1 as the pathogen recognition receptor being required for Syk-dependent Tec activation. Hence, Tec is a novel innate-specific inflammatory kinase, whose genetic ablation or inhibition by small molecule drugs strongly protects mice from fungal sepsis. These data demonstrate a therapeutic potential for Tec kinase inhibition to combat invasive microbial infections by attenuating the host inflammatory response.

Indexed as

AnimalsCaspase 8Dectin-1Enzyme ActivationHumansInflammasomesInterleukin-1betaIntracellular Signaling Peptides and ProteinsLectins, C-TypeMiceMice, KnockoutMycosesProtein-Tyrosine KinasesSepsisSyk KinaseCasp8 protein, mouseCaspase 8Dectin-1IL1B protein, mouseInflammasomesInterleukin-1betaIntracellular Signaling Peptides and ProteinsLectins, C-TypeProtein-Tyrosine KinasesSyk KinaseSYK protein, humanSyk protein, mouseTec protein-tyrosine kinase

Identifiers

PMID25474208
PMCPMC4256681
OpenAlexW2041055293

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.