Evidence map›Paper›PMID 31138793›Full record

ArticleNature communications2019

Bcl10-controlled Malt1 paracaspase activity is key for the immune suppressive function of regulatory T cells.

Marc Rosenbaum, Andreas Gewies, Konstanze Pechloff, Christoph Heuser, Thomas Engleitner, Torben Gehring, Lara Hartjes, Sabrina Krebs, Daniel Krappmann, Mark Kriegsmann and 4 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.

0numbers the graph read from it
0cells of the map it votes in
63citing papers in PubMed
4.6field-weighted citation impact, top 4% 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

63 citing papers in PubMed, 82 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. A novel linker region truncating variant in BCL10 underlies a leaky immunodeficiency phenotype.Pediatric allergy and immunology : official publication of the European Society of Pediatric Allergy and Immunology · 2026
    Article
  6. Article
  7. Regulatory T cells in cancer and inflammation.Signal transduction and targeted therapy · 2026
    Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. NF-κB in inflammation and cancer.Cellular & molecular immunology · 2025
    Review
  15. Article
  16. Article
  17. Article
  18. Enforced CARD11/MALT1 signaling in dendritic cells triggers hemophagocytic lymphohistiocytosis.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  19. Article
  20. Article

3 more citing papers are in PubMed but not listed here.

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

14 authors at 5 institutions in 1 country.

Marc RosenbaumInstitute of Clinical Chemistry and Pathobiochemistry, TUM School of Medicine, Technical University of Munich, 81675, Munich, Germany.ORCID http://orcid.org/0000-0001-6834-385X
Andreas GewiesInstitute of Clinical Chemistry and Pathobiochemistry, TUM School of Medicine, Technical University of Munich, 81675, Munich, Germany.
Konstanze PechloffInstitute of Clinical Chemistry and Pathobiochemistry, TUM School of Medicine, Technical University of Munich, 81675, Munich, Germany.
Christoph HeuserTranslaTUM, Center for Translational Cancer Research, Technical University of Munich, 81675, Munich, Germany.ORCID http://orcid.org/0000-0003-1410-7573
Thomas EngleitnerTranslaTUM, Center for Translational Cancer Research, Technical University of Munich, 81675, Munich, Germany.
Torben GehringResearch Unit Cellular Signal Integration, Helmholtz Zentrum München, German Research Center for Environmental Health, 85764, Neuherberg, Germany.
Lara HartjesInstitute of Clinical Chemistry and Pathobiochemistry, TUM School of Medicine, Technical University of Munich, 81675, Munich, Germany.
Sabrina KrebsInstitute of Clinical Chemistry and Pathobiochemistry, TUM School of Medicine, Technical University of Munich, 81675, Munich, Germany.
Daniel KrappmannResearch Unit Cellular Signal Integration, Helmholtz Zentrum München, German Research Center for Environmental Health, 85764, Neuherberg, Germany.
Mark KriegsmannInstitute of Pathology, University Hospital Heidelberg, 69120, Heidelberg, Germany.
Wilko WeichertInstitute of Pathology, Technical University of Munich, 81675, Munich, Germany.
Roland RadTranslaTUM, Center for Translational Cancer Research, Technical University of Munich, 81675, Munich, Germany.
Christian KurtsInstitute of Experimental Immunology, Rheinische-Friedrichs-Wilhelms University of Bonn, 53127, Bonn, Germany.ORCID http://orcid.org/0000-0002-6620-2401
Jürgen RulandInstitute of Clinical Chemistry and Pathobiochemistry, TUM School of Medicine, Technical University of Munich, 81675, Munich, Germany. j.ruland@tum.de.ORCID http://orcid.org/0000-0002-8381-3597
Technical University of Munich · DEGerman Cancer Research Center · DEHelmholtz Zentrum München · DEUniversity of Bonn · DEHeidelberg University · DE

Funding

Deutsche Forschungsgemeinschaft (German Research Foundation) RU 695/9-1Deutsche Forschungsgemeinschaft (German Research Foundation) SFB 1054/A04, B01Deutsche Forschungsgemeinschaft (German Research Foundation) SFB 1335/P01, P07, P08Deutsche Forschungsgemeinschaft (German Research Foundation) SFB 1371/P05Deutsche Forschungsgemeinschaft (German Research Foundation) TRR 237/A10, B15EC | EU Framework Programme for Research and Innovation H2020 | H2020 Priority Excellent Science | H2020 European Research Council (H2020 Excellent Science - European Research Council) 322865
6 · The paper itself

Abstract

Regulatory T cells (Tregs) have crucial functions in the inhibition of immune responses. Their development and suppressive functions are controlled by the T cell receptor (TCR), but the TCR signaling mechanisms that mediate these effects remain ill-defined. Here we show that CARD11-BCL10-MALT1 (CBM) signaling mediates TCR-induced NF-κB activation in Tregs and controls the conversion of resting Tregs to effector Tregs under homeostatic conditions. However, in inflammatory milieus, cytokines can bypass the CBM requirement for this differentiation step. By contrast, CBM signaling, in a MALT1 protease-dependent manner, is essential for mediating the suppressive function of Tregs. In malignant melanoma models, acute genetic blockade of BCL10 signaling selectively in Tregs or pharmacological MALT1 inhibition enhances anti-tumor immune responses. Together, our data uncover a segregation of Treg differentiation and suppressive function at the CBM complex level, and provide a rationale to explore MALT1 inhibitors for cancer immunotherapy.

Indexed as

AnimalsB-Cell CLL-Lymphoma 10 ProteinCARD Signaling Adaptor ProteinsCell DifferentiationCytokinesMelanoma, ExperimentalMiceMucosa-Associated Lymphoid Tissue Lymphoma Translocation 1 ProteinNF-kappa BReceptors, Antigen, T-CellSignal TransductionT-Lymphocytes, RegulatoryT-Lymphocyte SubsetsB-Cell CLL-Lymphoma 10 ProteinBcl10 protein, mouseCard11 protein, mouseCARD Signaling Adaptor ProteinsCytokinesMucosa-Associated Lymphoid Tissue Lymphoma Translocation 1 ProteinNF-kappa BReceptors, Antigen, T-Cell

Identifiers

PMID31138793
PMCPMC6538646
OpenAlexW2947026234

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.