Evidence map›Paper›PMID 28452361›Full record

ArticleNature communications2017

Elevated levels of Bcl-3 inhibits Treg development and function resulting in spontaneous colitis.

Sonja Reißig, Yilang Tang, Alexei Nikolaev, Katharina Gerlach, Christine Wolf, Kathrin Davari, Christian Gallus, Joumana Masri, Ilgiz A Mufazalov, Markus F Neurath and 7 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.0field-weighted citation impact, top 26% 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

20 citing papers in PubMed, 33 citations in OpenAlex.

  1. Unveiling the multifaceted roles of BCL3: biological functions and disease implications.Apoptosis : an international journal on programmed cell death · 2026
    Review
  2. Regulation and Function of the Atypical IκBs-Bcl-3, IκBEuropean journal of immunology · 2025
    Review
  3. Review
  4. Article
  5. Article
  6. Lupus susceptibility geneScience advances · 2024
    Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. NF-κB in control of regulatory T cell development, identity, and function.Journal of molecular medicine (Berlin, Germany) · 2022
    Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. Bcl-3 suppresses differentiation of RORγtImmunology and cell biology · 2021
    Article
  18. Review
  19. Article
  20. Article
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

17 authors at 4 institutions in 1 country.

Sonja ReißigInstitute for Molecular Medicine, University Medical Center of the Johannes Gutenberg, University of Mainz, Obere Zahlbarer Str 67, 55131 Mainz, Germany.
Yilang TangInstitute for Molecular Medicine, University Medical Center of the Johannes Gutenberg, University of Mainz, Obere Zahlbarer Str 67, 55131 Mainz, Germany.ORCID 0000-0001-7560-8369
Alexei NikolaevInstitute for Molecular Medicine, University Medical Center of the Johannes Gutenberg, University of Mainz, Obere Zahlbarer Str 67, 55131 Mainz, Germany.
Katharina GerlachDepartment of Medicine I, University Erlangen-Nürnberg, Research Campus, 91052 Erlangen, Germany.
Christine WolfHelmholtz Zentrum München, Institute of Diabetes and Obesity (IDO), German Center for Diabetes Research (DZD), 85764 München-Neuherberg, Germany.
Kathrin DavariHelmholtz Zentrum München, Institute of Diabetes and Obesity (IDO), German Center for Diabetes Research (DZD), 85764 München-Neuherberg, Germany.
Christian GallusHelmholtz Zentrum München, Institute of Diabetes and Obesity (IDO), German Center for Diabetes Research (DZD), 85764 München-Neuherberg, Germany.
Joumana MasriInstitute for Molecular Medicine, University Medical Center of the Johannes Gutenberg, University of Mainz, Obere Zahlbarer Str 67, 55131 Mainz, Germany.
Ilgiz A MufazalovInstitute for Molecular Medicine, University Medical Center of the Johannes Gutenberg, University of Mainz, Obere Zahlbarer Str 67, 55131 Mainz, Germany.ORCID 0000-0001-9332-0131
Markus F NeurathDepartment of Medicine I, University Erlangen-Nürnberg, Research Campus, 91052 Erlangen, Germany.
F Thomas WunderlichMax Planck Institute for Metabolism Research, CECAD, CMMC, Institute for Genetics, 50931 Cologne, Germany.
Jörn M SchattenbergDepartment of Internal Medicine I, University Medical Center of the Johannes Gutenberg, University of Mainz, 55131 Mainz, Germany.
Peter R GalleDepartment of Internal Medicine I, University Medical Center of the Johannes Gutenberg, University of Mainz, 55131 Mainz, Germany.
Benno WeigmannDepartment of Medicine I, University Erlangen-Nürnberg, Research Campus, 91052 Erlangen, Germany.
Ari WaismanInstitute for Molecular Medicine, University Medical Center of the Johannes Gutenberg, University of Mainz, Obere Zahlbarer Str 67, 55131 Mainz, Germany.ORCID 0000-0003-4304-8234
Elke GlasmacherHelmholtz Zentrum München, Institute of Diabetes and Obesity (IDO), German Center for Diabetes Research (DZD), 85764 München-Neuherberg, Germany.
Nadine HövelmeyerInstitute for Molecular Medicine, University Medical Center of the Johannes Gutenberg, University of Mainz, Obere Zahlbarer Str 67, 55131 Mainz, Germany.
Johannes Gutenberg University Mainz · DEHelmholtz Zentrum München · DEFriedrich-Alexander-Universität Erlangen-Nürnberg · DEMax Planck Institute for Metabolism Research · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Bcl-3 is an atypical NF-κB family member that regulates NF-κB-dependent gene expression in effector T cells, but a cell-intrinsic function in regulatory T (Treg) cells and colitis is not clear. Here we show that Bcl-3 expression levels in colonic T cells correlate with disease manifestation in patients with inflammatory bowel disease. Mice with T-cell-specific overexpression of Bcl-3 develop severe colitis that can be attributed to defective Treg cell development and function, leading to the infiltration of immune cells such as pro-inflammatory γδT cells, but not αβ T cells. In Treg cells, Bcl-3 associates directly with NF-κB p50 to inhibit DNA binding of p50/p50 and p50/p65 NF-κB dimers, thereby regulating NF-κB-mediated gene expression. This study thus reveals intrinsic functions of Bcl-3 in Treg cells, identifies Bcl-3 as a potential prognostic marker for colitis and illustrates the mechanism by which Bcl-3 regulates NF-κB activity in Tregs to prevent colitis.

Indexed as

AdultAnimalsB-Cell Lymphoma 3 ProteinColitisFemaleGene Expression RegulationHEK293 CellsHumansMaleMice, Inbred C57BLMice, KnockoutMiddle AgedNF-kappa BNF-kappa B p50 SubunitProtein BindingProto-Oncogene ProteinsB-Cell Lymphoma 3 ProteinBCL3 protein, humanBcl3 protein, mouseNF-kappa BNF-kappa B p50 SubunitProto-Oncogene ProteinsRELA protein, humanTranscription Factor RelATranscription Factors

Identifiers

PMID28452361
PMCPMC5414353
OpenAlexW2609297019

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.