Evidence map›Paper›PMID 27114609›Full record

ArticleThe Journal of experimental medicine2016

Continuous inhibitory signaling by both SHP-1 and SHIP-1 pathways is required to maintain unresponsiveness of anergic B cells.

Andrew Getahun, Nicole A Beavers, Sandy R Larson, Mark J Shlomchik, John C Cambier

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers.

0numbers the graph read from it
0cells of the map it votes in
81citing papers in PubMed
7.0field-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

81 citing papers in PubMed, 103 citations in OpenAlex.

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  17. Polysaccharide fromInternational journal of molecular sciences · 2024
    Article
  18. Serum immunoglobulin and the threshold of Fc receptor-mediated immune activation.Biochimica et biophysica acta. General subjects · 2023
    Review
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21 more citing papers are in PubMed but not listed here.

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

5 authors at 3 institutions in 1 country.

Andrew GetahunDepartment of Immunology and Microbiology, University of Colorado School of Medicine, Aurora, CO 80045 Department of Biomedical Research, National Jewish Health, Denver, CO 80206.
Nicole A BeaversDepartment of Immunology and Microbiology, University of Colorado School of Medicine, Aurora, CO 80045 Department of Biomedical Research, National Jewish Health, Denver, CO 80206.
Sandy R LarsonDepartment of Immunology and Microbiology, University of Colorado School of Medicine, Aurora, CO 80045 Department of Biomedical Research, National Jewish Health, Denver, CO 80206.
Mark J ShlomchikDepartment of Immunology, University of Pittsburgh School of Medicine, Pittsburgh, PA 15261.
John C CambierDepartment of Immunology and Microbiology, University of Colorado School of Medicine, Aurora, CO 80045 Department of Biomedical Research, National Jewish Health, Denver, CO 80206 John.Cambier@ucdenver.edu.
National Jewish Health · USUniversity of Colorado Denver · USUniversity of Pittsburgh · US

Funding

THE REGULATION OF V ALPHA 7 EXPRESSING T CELLSP01AI022295 · NIAID · NATIONAL JEWISH HEALTH · PI REFAELI, YOSEF · 1985 to 2011
$11.7M
Signaling and Selection in Germinal Center B CellsR01AI105018 · NIAID · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI MARK J SHLOMCHIK · 2014 to 2026
$4.8M
Autoimmunity risk alleles compromising B cell anergyR01AI124487 · NIAID · UNIVERSITY OF COLORADO DENVER · PI CAMBIER, JOHN C · 2016 to 2020
$2.5M
Infectious Agents and B Cell AnergyR01AI077597 · NIAID · UNIVERSITY OF COLORADO DENVER · PI CAMBIER, JOHN C · 2010 to 2014
$1.9M
B Cells and Type 1 DiabetesR01DK096492 · NIDDK · UNIVERSITY OF COLORADO DENVER · PI CAMBIER, JOHN C · 2012 to 2016
$1.6M
NIAID NIH HHS P01 AI022295NIAID NIH HHS R01 AI077597NIAID NIH HHS R01 AI105018NIAID NIH HHS R01 AI124487NIDDK NIH HHS R01 DK096492
6 · The paper itself

Abstract

Many autoreactive B cells persist in the periphery in a state of unresponsiveness called anergy. This unresponsiveness is rapidly reversible, requiring continuous BCR interaction with self-antigen and resultant regulatory signaling for its maintenance. Using adoptive transfer of anergic B cells with subsequent acute induction of gene deletion or expression, we demonstrate that the continuous activities of independent inhibitory signaling pathways involving the tyrosine phosphatase SHP-1 and the inositol phosphatase SHIP-1 are required to maintain anergy. Acute breach of anergy by compromise of either of these pathways leads to rapid cell activation, proliferation, and generation of short-lived plasma cells that reside in extrafollicular foci. Results are consistent with predicted/observed reduction in the Lyn-SHIP-1-PTEN-SHP-1 axis function in B cells from systemic lupus erythematosus patients.

Indexed as

Clonal AnergyAnimalsB-LymphocytesHumansLupus Erythematosus, SystemicMiceMice, TransgenicPhosphatidylinositol-3,4,5-Trisphosphate 5-PhosphatasesProtein Tyrosine Phosphatase, Non-Receptor Type 6PTEN PhosphohydrolaseSignal Transductionsrc-Family KinasesINPP5D protein, humanlyn protein-tyrosine kinasePhosphatidylinositol-3,4,5-Trisphosphate 5-PhosphatasesProtein Tyrosine Phosphatase, Non-Receptor Type 6PTEN PhosphohydrolasePten protein, mousesrc-Family Kinases

Identifiers

PMID27114609
PMCPMC4854724
OpenAlexW2344712410

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.