Evidence map›Paper›PMID 27428827›Full record

ArticleNature immunology2016

Autonomous membrane IgE signaling prevents IgE-memory formation.

Kei Haniuda, Saori Fukao, Tadahiro Kodama, Hitoshi Hasegawa, Daisuke Kitamura

Abstract read
PubMed Publisher
In one paragraph

Article in Nature immunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers.

0numbers the graph read from it
0cells of the map it votes in
67citing papers in PubMed
6.2field-weighted citation impact, top 3% 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

67 citing papers in PubMed, 128 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Progressively differentiated TNature immunology · 2025
    Article
  11. Review
  12. Understanding and Managing Hyper IgE Syndromes.ImmunoTargets and therapy · 2025
    Review
  13. Whence and wherefore IgE?Immunological reviews · 2024
    Review
  14. Review
  15. Article
  16. Origins and diversity of pan-isotype human bone marrow plasma cells.bioRxiv : the preprint server for biology · 2024
    Article
  17. Article
  18. Review
  19. Review
  20. Article

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

Kei HaniudaDivision of Molecular Biology, Research Institute for Biomedical Sciences, Tokyo University of Science, Noda, Japan.
Saori FukaoDivision of Molecular Biology, Research Institute for Biomedical Sciences, Tokyo University of Science, Noda, Japan.
Tadahiro KodamaDivision of Molecular Biology, Research Institute for Biomedical Sciences, Tokyo University of Science, Noda, Japan.
Hitoshi HasegawaDivision of Molecular Biology, Research Institute for Biomedical Sciences, Tokyo University of Science, Noda, Japan.
Daisuke KitamuraDivision of Molecular Biology, Research Institute for Biomedical Sciences, Tokyo University of Science, Noda, Japan.
Tokyo University of Science · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Aberrant production of IgE antibodies can lead to allergic diseases. Normally, IgE(+) B cells rarely differentiate into memory B cells (Bmem) or long-lived plasma cells (LLPCs), as they only transiently participate in the germinal center (GC), but the mechanism behind this remains elusive. We found that membrane IgE (mIgE) autonomously triggered rapid plasma-cell differentiation and apoptosis independently of antigen or cellular context, predominantly through the mutually independent CD19-PI3K-Akt-IRF4 and BLNK-Jnk/p38 pathways, respectively, and we identified the ectodomains of mIgE as being responsible. Accordingly, deregulated GC IgE(+) B cell proliferation and prolonged IgE production with exaggerated anaphylaxis were observed in CD19- and BLNK-deficient mice. Our findings reveal an autonomous mIgE signaling mechanism that normally prevents IgE(+) Bmem and LLPC formation, providing insights into the molecular pathogenesis of allergic diseases.

Indexed as

Cell MembraneImmunologic Memory3T3 CellsAnaphylaxisAnimalsAntigens, CD19ApoptosisB-LymphocytesCalcium SignalingCell DifferentiationCell ProliferationEnzyme-Linked Immunospot AssayGerminal CenterHypersensitivityImmunoglobulin Class SwitchingImmunoglobulin EAntigens, CD19Immunoglobulin EImmunoglobulin GReceptors, Antigen, B-Cell

Identifiers

PMID27428827
OpenAlexW2481181469

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.