Evidence map›Paper›PMID 25225457›Full record

ArticleThe Journal of experimental medicine2014

IKK-induced NF-κB1 p105 proteolysis is critical for B cell antibody responses to T cell-dependent antigen.

Emilie Jacque, Edina Schweighoffer, Alexander Visekruna, Stamatia Papoutsopoulou, Julia Janzen, Rachel Zillwood, David M Tarlinton, Victor L J Tybulewicz, Steven C Ley

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.6field-weighted citation impact, top 18% 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

19 citing papers in PubMed, 28 citations in OpenAlex.

  1. Article
  2. Review
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  4. Article
  5. Cell adhesion tunes inflammatory TPL2 kinase signal transduction.Cellular and molecular life sciences : CMLS · 2022
    Article
  6. Article
  7. Review
  8. Review
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  18. Article
  19. Dynamics of B cells in germinal centres.Nature reviews. Immunology · 2015
    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

9 authors at 1 institution in 1 country.

Emilie JacqueDivision of Immune Cell Biology, MRC National Institute for Medical Research, London NW7 1AA, England, UK.
Edina SchweighofferDivision of Immune Cell Biology, MRC National Institute for Medical Research, London NW7 1AA, England, UK.
Alexander VisekrunaDivision of Immune Cell Biology, MRC National Institute for Medical Research, London NW7 1AA, England, UK.
Stamatia PapoutsopoulouDivision of Immune Cell Biology, MRC National Institute for Medical Research, London NW7 1AA, England, UK.
Julia JanzenDivision of Immune Cell Biology, MRC National Institute for Medical Research, London NW7 1AA, England, UK.
Rachel ZillwoodDivision of Immune Cell Biology, MRC National Institute for Medical Research, London NW7 1AA, England, UK.
David M TarlintonThe Walter and Eliza Hall Institute for Medical Research, Parkville, Victoria 3052, Australia.
Victor L J TybulewiczDivision of Immune Cell Biology, MRC National Institute for Medical Research, London NW7 1AA, England, UK.
Steven C LeyDivision of Immune Cell Biology, MRC National Institute for Medical Research, London NW7 1AA, England, UK sley@nimr.mrc.ac.uk.
Walter and Eliza Hall Institute of Medical Research · AU

Funding

Medical Research Council MC_U117527252Medical Research Council MC_U117584209
6 · The paper itself

Abstract

The importance of IκB kinase (IKK)-induced proteolysis of NF-κB1 p105 in B cells was investigated using Nfkb1(SSAA/SSAA) mice, in which this NF-κB signaling pathway is blocked. Nfkb1(SSAA) mutation had no effect on the development and homeostasis of follicular mature (FM) B cells. However, analysis of mixed bone marrow chimeras revealed that Nfkb1(SSAA/SSAA) FM B cells were completely unable to mediate T cell-dependent antibody responses. Nfkb1(SSAA) mutation decreased B cell antigen receptor (BCR) activation of NF-κB in FM B cells, which selectively blocked BCR stimulation of cell survival and antigen-induced differentiation into plasmablasts and germinal center B cells due to reduced expression of Bcl-2 family proteins and IRF4, respectively. In contrast, the antigen-presenting function of FM B cells and their BCR-induced migration to the follicle T cell zone border, as well as their growth and proliferation after BCR stimulation, were not affected. All of the inhibitory effects of Nfkb1(SSAA) mutation on B cell functions were rescued by normalizing NF-κB activation genetically. Our study identifies critical B cell-intrinsic functions for IKK-induced NF-κB1 p105 proteolysis in the antigen-induced survival and differentiation of FM B cells, which are essential for T-dependent antibody responses.

Indexed as

AnimalsAntibody FormationB-LymphocytesFlow CytometryI-kappa B KinaseImmunoblottingMiceMice, KnockoutMicroscopy, FluorescenceMutationNF-kappa B p50 SubunitProteolysisReal-Time Polymerase Chain ReactionReceptors, Antigen, B-CellSignal TransductionStatistics, NonparametricI-kappa B KinaseNF-kappa B p50 SubunitReceptors, Antigen, B-Cell

Identifiers

PMID25225457
PMCPMC4172221
OpenAlexW2131367318

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.