Evidence map›Paper›PMID 23135975›Full record

ArticleEuropean journal of immunology2013

Aberrant antibody affinity selection in SHIP-deficient B cells.

Wai-Hang Leung, Tatiana Tarasenko, Zuzana Biesova, Hemanta Kole, Elizabeth R Walsh, Silvia Bolland

Open access · bronzeAbstract read
In one paragraph

Article in European journal of immunology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.0field-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

15 citing papers in PubMed, 28 citations in OpenAlex.

  1. Article
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  5. Excessive CD11cProceedings of the National Academy of Sciences of the United States of America · 2019
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  6. Article
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  8. Targeting B cells in treatment of autoimmunity.Current opinion in immunology · 2016
    Review
  9. Article
  10. Article
  11. Signaling mechanisms regulating B-lymphocyte activation and tolerance.Journal of molecular medicine (Berlin, Germany) · 2015
    Review
  12. Actin-binding protein 1 links B-cell antigen receptors to negative signaling pathways.Proceedings of the National Academy of Sciences of the United States of America · 2014
    Article
  13. Article
  14. Review
  15. 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

6 authors at 2 institutions in 1 country.

Wai-Hang LeungLaboratory of Immunogenetics, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, MD, USA.
Tatiana Tarasenko
Zuzana Biesova
Hemanta Kole
Elizabeth R Walsh
Silvia Bolland
National Institute of Allergy and Infectious Diseases · USNational Institutes of Health · US

Funding

Genetic Modifiers Of Autoimmune Disease In FcgammaRIIB Mutant MiceZIAAI000912 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI BOLLAND, SILVIA · 2009 to 2025
$27.0M
Regulation Of The Immune Response By The Inositol Phosphatase SHIPZIAAI000911 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI BOLLAND, SILVIA · 2009 to 2010
$581k
Intramural NIH HHS ZIA AI000911
6 · The paper itself

Abstract

The strength of the Ag receptor signal influences development and negative selection of B cells, and it might also affect B-cell survival and selection in the GC. Here, we have used mice with B-cell-specific deletion of the 5'-inositol phosphatase SHIP as a model to study affinity selection in cells that are hyperresponsive to Ag and cytokine receptor stimulation. In the absence of SHIP, B cells have lower thresholds for Ag- and interferon (IFN)-induced activation, resulting in augmented negative selection in the BM and enhanced B-cell maturation in the periphery. Despite a tendency to spontaneously downregulate surface IgM expression, SHIP deficiency does not alter anergy induction in response to soluble hen-egg lysozyme Ag in the MDA4 transgenic model. SHIP-deficient B cells spontaneously produce isotype-switched antibodies; however, they are poor responders in immunization and infection models. While SHIP-deficient B cells form GCs and undergo mutation, they are not properly selected for high-affinity antibodies. These results illustrate the importance of negative regulation of B-cell responses, as lower thresholds for B-cell activation promote survival of low affinity and deleterious receptors to the detriment of optimal Ab affinity maturation.

Indexed as

AnimalsAntibody AffinityAntigensB-LymphocytesImmunoglobulin GImmunoglobulin MInositol Polyphosphate 5-PhosphatasesInterferonsMiceMice, Inbred C57BLMice, TransgenicPhosphoric Monoester HydrolasesReceptors, AntigenT-LymphocytesAntigensImmunoglobulin GImmunoglobulin MInositol Polyphosphate 5-PhosphatasesInterferonsPhosphoric Monoester HydrolasesReceptors, Antigen

Identifiers

PMID23135975
PMCPMC3903325
OpenAlexW1927916230

What OpenQuestion holds

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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.