Evidence map›Paper›PMID 27099294›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2016

Canonical NF-κB signaling is uniquely required for the long-term persistence of functional mature B cells.

Emmanuel Derudder, Sebastian Herzog, Verena Labi, Tomoharu Yasuda, Karl Köchert, Martin Janz, Andreas Villunger, Marc Schmidt-Supprian, Klaus Rajewsky

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2016. 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
1.4field-weighted citation impact, top 20% 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, 26 citations in OpenAlex.

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  8. Research progress on inflammatory mechanism of primary Sjögren syndrome.Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2021
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  14. PTIP chromatin regulator controls development and activation of B cell subsets to license humoral immunity in mice.Proceedings of the National Academy of Sciences of the United States of America · 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

9 authors at 4 institutions in 3 countries.

Emmanuel DerudderProgram of Cellular and Molecular Medicine, Children's Hospital, Harvard Medical School, Boston, MA 02115; Immune Disease Institute, Harvard Medical School, Boston, MA 02115; Max Delbrück Center for Molecular Medicine, 13125 Berlin, Germany;
Sebastian HerzogDivision of Developmental Immunology, Biocenter, Medical University Innsbruck, 6020 Innsbruck, Austria;
Verena LabiMax Delbrück Center for Molecular Medicine, 13125 Berlin, Germany;
Tomoharu YasudaMax Delbrück Center for Molecular Medicine, 13125 Berlin, Germany;
Karl KöchertMax Delbrück Center for Molecular Medicine, 13125 Berlin, Germany;
Martin JanzMax Delbrück Center for Molecular Medicine, 13125 Berlin, Germany; Hematology, Oncology, and Tumor Immunology, Charité-University Hospital Berlin, Campus Benjamin Franklin, 12200 Berlin, Germany;
Andreas VillungerDivision of Developmental Immunology, Biocenter, Medical University Innsbruck, 6020 Innsbruck, Austria; Tyrolean Cancer Research Institute, 6020 Innsbruck, Austria;
Marc Schmidt-SupprianProgram of Cellular and Molecular Medicine, Children's Hospital, Harvard Medical School, Boston, MA 02115; Immune Disease Institute, Harvard Medical School, Boston, MA 02115; Department of Hematology and Oncology, Klinikum Rechts der Isar, Technische Universität München, 81675 Munich, Germany.
Klaus RajewskyProgram of Cellular and Molecular Medicine, Children's Hospital, Harvard Medical School, Boston, MA 02115; Immune Disease Institute, Harvard Medical School, Boston, MA 02115; Max Delbrück Center for Molecular Medicine, 13125 Berlin, Germany; klaus.rajewsky@mdc-berlin.de.
Max Delbrück Center · DEHarvard University · USInnsbruck Medical University · ATTyrolean Cancer Research Institute · AT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although canonical NF-κB signaling is crucial to generate a normal mature B-cell compartment, its role in the persistence of resting mature B cells is controversial. To resolve this conflict, we ablated NF-κB essential modulator (NEMO) and IκB kinase 2 (IKK2), two essential mediators of the canonical pathway, either early on in B-cell development or specifically in mature B cells. Early ablation severely inhibited the generation of all mature B-cell subsets, but follicular B-cell numbers could be largely rescued by ectopic expression of B-cell lymphoma 2 (Bcl2), despite a persisting block at the transitional stage. Marginal zone (MZ) B and B1 cells were not rescued, indicating a possible role of canonical NF-κB signals beyond the control of cell survival in these subsets. When canonical NF-κB signaling was ablated specifically in mature B cells, the differentiation and/or persistence of MZ B cells was still abrogated, but follicular B-cell numbers were only mildly affected. However, the mutant cells exhibited increased turnover as well as functional deficiencies upon activation, suggesting that canonical NF-κB signals contribute to their long-term persistence and functional fitness.

Indexed as

AnimalsB-LymphocytesCells, CulturedCell SurvivalMiceMice, Inbred C57BLNF-kappa BSignal TransductionNF-kappa Bcanonical signalingfollicular B cellsNF-κBpersistence

Identifiers

PMID27099294
PMCPMC4983837
OpenAlexW2338331339

What OpenQuestion holds

Textmetadata
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.