Evidence map›Paper›PMID 36880536›Full record

ArticleThe Journal of experimental medicine2023

B cell receptor ligation induces IgE plasma cell elimination.

Adam K Wade-Vallance, Zhiyong Yang, Jeremy B Libang, Marcus J Robinson, David M Tarlinton, Christopher D C Allen

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

14 citing papers in PubMed, 21 citations in OpenAlex.

  1. Review
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  7. Review
  8. Polarization of the memory B-cell response.Journal of leukocyte biology · 2025
    Review
  9. Whence and wherefore IgE?Immunological reviews · 2024
    Review
  10. Article
  11. Review
  12. Article
  13. Review
  14. 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

6 authors at 2 institutions in 2 countries.

Adam K Wade-VallanceBiomedical Sciences Graduate Program, University of California, San Francisco , San Francisco, CA, USA.ORCID 0000-0002-6863-1461
Zhiyong YangCardiovascular Research Institute, University of California, San Francisco , San Francisco, CA, USA.ORCID 0000-0003-0589-6224
Jeremy B LibangCardiovascular Research Institute, University of California, San Francisco , San Francisco, CA, USA.ORCID 0000-0001-8678-8131
Marcus J RobinsonCardiovascular Research Institute, University of California, San Francisco , San Francisco, CA, USA.ORCID 0000-0001-5677-3078
David M TarlintonDepartment of Immunology and Pathology, Monash University , Melbourne, Australia.ORCID 0000-0001-9928-686X
Christopher D C AllenCardiovascular Research Institute, University of California, San Francisco , San Francisco, CA, USA.ORCID 0000-0002-1879-9047
University of California, San Francisco · USMonash University · AU

Funding

Translational InformaticsP30CA082103 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI Kate Taylor Shumate · 1999 to 2026
$209.7M
Virology CoreP30AI027763 · NIAID · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI MALLORY O JOHNSON · 1988 to 2026
$93.6M
Regulation of IgE responses by B cell receptor signalingR01AI130470 · NIAID · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI ALLEN, CHRISTOPHER DAVID CABALLERO · 2018 to 2022
$2.0M
Post Baccalaureate Research Opportunity To Promote Equity In Learning (PROPEL).R25GM144250 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI Ryan D. Hernandez, Todd Nystul · 2022 to 2026
$1.8M
NCI NIH HHS P30 CA082103NIAID NIH HHS P30 AI027763NIAID NIH HHS R01 AI130470NIGMS NIH HHS R25 GM144250
6 · The paper itself

Abstract

The proper regulation of IgE production safeguards against allergic disease, highlighting the importance of mechanisms that restrict IgE plasma cell (PC) survival. IgE PCs have unusually high surface B cell receptor (BCR) expression, yet the functional consequences of ligating this receptor are unknown. Here, we found that BCR ligation induced BCR signaling in IgE PCs followed by their elimination. In cell culture, exposure of IgE PCs to cognate antigen or anti-BCR antibodies induced apoptosis. IgE PC depletion correlated with the affinity, avidity, amount, and duration of antigen exposure and required the BCR signalosome components Syk, BLNK, and PLCγ2. In mice with a PC-specific impairment of BCR signaling, the abundance of IgE PCs was selectively increased. Conversely, BCR ligation by injection of cognate antigen or anti-IgE depleted IgE PCs. These findings establish a mechanism for the elimination of IgE PCs through BCR ligation. This has important implications for allergen tolerance and immunotherapy as well as anti-IgE monoclonal antibody treatments.

Indexed as

HypersensitivityPlasma CellsAnimalsApoptosisCell NucleusCell SurvivalImmunosuppressive AgentsMiceReceptors, Antigen, B-CellImmunosuppressive AgentsReceptors, Antigen, B-Cell

Identifiers

PMID36880536
PMCPMC9997509
OpenAlexW4323347328

What OpenQuestion holds

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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.