Evidence map›Paper›PMID 35388002›Full record

ArticleNature communications2022

Phagosomal signalling of the C-type lectin receptor Dectin-1 is terminated by intramembrane proteolysis.

Torben Mentrup, Anna Yamina Stumpff-Niggemann, Nadja Leinung, Christine Schlosser, Katja Schubert, Rebekka Wehner, Antje Tunger, Valentin Schatz, Patrick Neubert, Ann-Christine Gradtke and 9 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
6.7field-weighted citation impact, top 3% 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

17 citing papers in PubMed, 34 citations in OpenAlex.

  1. Article
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  6. Structural insights into human signal peptide peptidase.Proceedings of the National Academy of Sciences of the United States of America · 2025
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  10. Review
  11. Article
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  14. Preparation ofACS applied bio materials · 2023
    Article
  15. Article
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  17. 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

19 authors at 7 institutions in 1 country.

Torben MentrupInstitute of Physiological Chemistry, Faculty of Medicine Carl Gustav Carus, Technische Universität Dresden, Dresden, Germany.ORCID 0000-0003-4570-8734
Anna Yamina Stumpff-NiggemannBiochemical Institute, Christian-Albrechts-University of Kiel, Kiel, Germany.
Nadja LeinungInstitute of Physiological Chemistry, Faculty of Medicine Carl Gustav Carus, Technische Universität Dresden, Dresden, Germany.
Christine SchlosserBiochemistry and Molecular Biology, Institute of Theoretical Medicine, Medical Faculty, University of Augsburg, Augsburg, Germany.
Katja SchubertResearch Group Microbial Immunology, Leibniz Institute for Natural Product Research and Infection Biology, Hans Knöll Institute, Jena, Germany.
Rebekka WehnerInstitute of Immunology, Faculty of Medicine Carl Gustav Carus, Technische Universität Dresden, Dresden, Germany.
Antje TungerInstitute of Immunology, Faculty of Medicine Carl Gustav Carus, Technische Universität Dresden, Dresden, Germany.
Valentin SchatzInstitute of Clinical Microbiology and Hygiene, University Hospital of Regensburg and University of Regensburg, Regensburg, Germany.
Patrick NeubertInstitute of Clinical Microbiology and Hygiene, University Hospital of Regensburg and University of Regensburg, Regensburg, Germany.
Ann-Christine GradtkeInstitute of Physiological Chemistry, Faculty of Medicine Carl Gustav Carus, Technische Universität Dresden, Dresden, Germany.
Janina WolfBiochemical Institute, Christian-Albrechts-University of Kiel, Kiel, Germany.
Stefan Rose-JohnBiochemical Institute, Christian-Albrechts-University of Kiel, Kiel, Germany.ORCID 0000-0002-7519-3279
Paul SaftigBiochemical Institute, Christian-Albrechts-University of Kiel, Kiel, Germany.ORCID 0000-0003-2637-7052
Alexander DalpkeInstitute of Medical Microbiology and Virology, University Hospital Carl Gustav Carus, Medical Faculty, Technische Universität Dresden, Dresden, Germany.
Jonathan JantschInstitute of Clinical Microbiology and Hygiene, University Hospital of Regensburg and University of Regensburg, Regensburg, Germany.
Marc SchmitzInstitute of Immunology, Faculty of Medicine Carl Gustav Carus, Technische Universität Dresden, Dresden, Germany.
Regina FluhrerBiochemistry and Molecular Biology, Institute of Theoretical Medicine, Medical Faculty, University of Augsburg, Augsburg, Germany.ORCID 0000-0002-9778-4643
Ilse D JacobsenResearch Group Microbial Immunology, Leibniz Institute for Natural Product Research and Infection Biology, Hans Knöll Institute, Jena, Germany.
Bernd SchröderInstitute of Physiological Chemistry, Faculty of Medicine Carl Gustav Carus, Technische Universität Dresden, Dresden, Germany. bernd.schroeder@tu-dresden.de.ORCID 0000-0003-0774-6270
University Hospital Carl Gustav Carus · DEChristian-Albrechts-Universität zu Kiel · DEUniversity Hospital Regensburg · DEGerman Cancer Research Center · DELeibniz-Institut für Naturstoff-Forschung und Infektionsbiologie e. V. - Hans-Knöll-Institut (HKI) · DEUniversity of Augsburg · DENational Center for Tumor Diseases · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Sensing of pathogens by pattern recognition receptors (PRR) is critical to initiate protective host defence reactions. However, activation of the immune system has to be carefully titrated to avoid tissue damage necessitating mechanisms to control and terminate PRR signalling. Dectin-1 is a PRR for fungal β-glucans on immune cells that is rapidly internalised after ligand-binding. Here, we demonstrate that pathogen recognition by the Dectin-1a isoform results in the formation of a stable receptor fragment devoid of the ligand binding domain. This fragment persists in phagosomal membranes and contributes to signal transduction which is terminated by the intramembrane proteases Signal Peptide Peptidase-like (SPPL) 2a and 2b. Consequently, immune cells lacking SPPL2b demonstrate increased anti-fungal ROS production, killing capacity and cytokine responses. The identified mechanism allows to uncouple the PRR signalling response from delivery of the pathogen to degradative compartments and identifies intramembrane proteases as part of a regulatory circuit to control anti-fungal immune responses.

Indexed as

Lectins, C-TypeSignal TransductionDectin-1LigandsProteolysisReceptors, Pattern RecognitionDectin-1Lectins, C-TypeLigandsReceptors, Pattern Recognition

Identifiers

PMID35388002
PMCPMC8987071
OpenAlexW4223475744

What OpenQuestion holds

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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.