Evidence map›Paper›PMID 21900180›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2011

Impaired B cell development and function in the absence of IkappaBNS.

Maki Touma, Derin B Keskin, Fumiko Shiroki, Ibuki Saito, Shigeo Koyasu, Ellis L Reinherz, Linda K Clayton

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
0.7field-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

26 citing papers in PubMed, 42 citations in OpenAlex.

  1. Regulation and Function of the Atypical IκBs-Bcl-3, IκBEuropean journal of immunology · 2025
    Review
  2. Article
  3. Article
  4. Article
  5. IκBFrontiers in immunology · 2022
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. NF-κB and Its Regulators During Pregnancy.Frontiers in immunology · 2021
    Review
  11. Article
  12. Article
  13. Article
  14. A HypermorphicJournal of immunology (Baltimore, Md. : 1950) · 2018
    Article
  15. Article
  16. Article
  17. Article
  18. Article
  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

7 authors at 4 institutions in 2 countries.

Maki ToumaLaboratory of Immunobiology, Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA 02115, USA.
Derin B Keskin
Fumiko Shiroki
Ibuki Saito
Shigeo Koyasu
Ellis L Reinherz
Linda K Clayton
Harvard University · USKeio University · JPDana-Farber Cancer Institute · USNiigata University · JP

Funding

T CELL ANTIGEN RECOGNITIONR37AI019807 · NIAID · DANA-FARBER CANCER INSTITUTE · PI REINHERZ, ELLIS L · 1999 to 2008
$4.4M
Molecular analysis of thymic negative selectionR01AI051479 · NIAID · DANA-FARBER CANCER INSTITUTE · PI CLAYTON, LINDA KATHLEEN · 2003 to 2007
$1.8M
T Cell Antigen RecognitionR01AI019807 · NIAID · DANA-FARBER CANCER INSTITUTE · PI REINHERZ, ELLIS L · 1985 to 2010
$1.3M
T Cell Antigen RecognitionR56AI019807 · NIAID · DANA-FARBER CANCER INST · PI REINHERZ, ELLIS L · 2012 to 2012
$430k
NIAID NIH HHS AI19807NIAID NIH HHS AI51779NIAID NIH HHS R01 AI019807NIAID NIH HHS R01 AI051479NIAID NIH HHS R37 AI019807NIAID NIH HHS R56 AI019807
6 · The paper itself

Abstract

IκBNS has been identified as a member of the IκB family of NF-κB inhibitors, which undergoes induction upon TCR signaling. Mice carrying a targeted gene disruption of IκBNS demonstrate dysregulation of cytokines in T cells, macrophages, and dendritic cells. IκBNS mediates both positive and negative gene regulation, depending on individual cell type and/or cytokine. In this study, we demonstrate an additional role for IκBNS in the B cell lineage. B cells from IκBNS knockout (KO) mice were impaired in proliferative responses to LPS and anti-CD40. IgM and IgG3 Igs were drastically reduced in the serum of IκBNS KO mice, although IκBNS KO B cells exhibited a higher level of surface IgM than that found in wild-type mice. Switching to IgG3 was significantly reduced in IκBNS KO B cells. The in vitro induction of plasma cell development demonstrated that progression to Ab-secreting cells was impaired in IκBNS KO B cells. In agreement with this finding, the number of Ab-secreting cells in the spleens of IκBNS KO mice was reduced and production of Ag-specific Igs was lower in IκBNS KO mice after influenza infection as compared with wild-type mice. Additionally, IκBNS KO mice lacked B1 B cells and exhibited a reduction in marginal zone B cells. Thus, IκBNS significantly impacts the development and functions of B cells and plasma cells.

Indexed as

AnimalsB-LymphocytesCell DifferentiationCell SeparationEnzyme-Linked Immunosorbent AssayFlow CytometryImmunohistochemistryIntracellular Signaling Peptides and ProteinsLymphocyte ActivationMiceMice, Inbred C57BLMice, KnockoutPlasma CellsProteinsReverse Transcriptase Polymerase Chain ReactionIntracellular Signaling Peptides and ProteinsNfkbid protein, mouseProteins

Identifiers

PMID21900180
PMCPMC3348541
OpenAlexW2100742549

What OpenQuestion holds

Textmetadata
LicenceTDM
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.