Evidence map›Paper›PMID 25630702›Full record

ArticleThe EMBO journal2015

CD19 and BAFF-R can signal to promote B-cell survival in the absence of Syk.

Elias Hobeika, Ella Levit-Zerdoun, Vasiliki Anastasopoulou, Roland Pohlmeyer, Simon Altmeier, Ameera Alsadeq, Marc-Werner Dobenecker, Roberta Pelanda, Michael Reth

Open access · bronzeAbstract read
In one paragraph

Article in The EMBO journal, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
5.3field-weighted citation impact, top 4% 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

46 citing papers in PubMed, 75 citations in OpenAlex.

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  12. Aberrant B-Cell Activation in Systemic Lupus Erythematosus.Kidney diseases (Basel, Switzerland) · 2022
    Review
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 6 institutions in 3 countries.

Elias HobeikaMax-Planck Institute of Immunobiology and Epigenetics, Freiburg, Germany Department of Molecular Immunology, BioIII, Faculty of Biology, Albert-Ludwigs-Universität Freiburg, Freiburg, Germany hobeika@ie-freiburg.mpg.de michael.reth@bioss.uni-freiburg.de.
Ella Levit-ZerdounMax-Planck Institute of Immunobiology and Epigenetics, Freiburg, Germany.
Vasiliki AnastasopoulouInstitute of Immunology, Charité Campus Buch, Berlin, Germany.
Roland PohlmeyerMax-Planck Institute of Immunobiology and Epigenetics, Freiburg, Germany.
Simon AltmeierInstitute of Mircobiology, Swiss Federal Institute of Technology, ETH Zurich, Zurich, Switzerland.
Ameera AlsadeqDepartment of General Pediatrics, University Medical Center Schleswig-Holstein, Kiel, Germany.
Marc-Werner DobeneckerLaboratory of Immune Cell Epigenetics and Signaling, The Rockefeller University, New York, NY, USA.
Roberta PelandaDepartment of Immunology and Microbiology, University of Colorado School of Medicine, Aurora, CO, USA.
Michael RethMax-Planck Institute of Immunobiology and Epigenetics, Freiburg, Germany Department of Molecular Immunology, BioIII, Faculty of Biology, Albert-Ludwigs-Universität Freiburg, Freiburg, Germany BIOSS, Centre For Biological Signaling Studies, University of Freiburg, Freiburg, Germany hobeika@ie-freiburg.mpg.de michael.reth@bioss.uni-freiburg.de.
Max Planck Society · DECharité - Universitätsmedizin Berlin · DEETH Zurich · CHMax Planck Institute of Immunobiology and Epigenetics · DERockefeller University · USUniversity of Colorado Denver · US

Funding

Tolerance in Polyclonal and Oligoclonal Immune SystemsR01AI052310 · NIAID · UNIVERSITY OF COLORADO DENVER · PI PELANDA, ROBERTA · 2003 to 2017
$5.0M
NIAID NIH HHS R01 AI052310
6 · The paper itself

Abstract

The development and function of B lymphocytes is regulated by numerous signaling pathways, some emanating from the B-cell antigen receptor (BCR). The spleen tyrosine kinase (Syk) plays a central role in the activation of the BCR, but less is known about its contribution to the survival and maintenance of mature B cells. We generated mice with an inducible and B-cell-specific deletion of the Syk gene and found that a considerable fraction of mature Syk-negative B cells can survive in the periphery for an extended time. Syk-negative B cells are defective in BCR, RP105 and CD38 signaling but still respond to an IL-4, anti-CD40, CpG or LPS stimulus. Our in vivo experiments show that Syk-deficient B cells require BAFF receptor and CD19/PI3K signaling for their long-term survival. These studies also shed a new light on the signals regulating the maintenance of the normal mature murine B-cell pool.

Indexed as

ADP-ribosyl Cyclase 1AnimalsAntibodiesAntigens, CDAntigens, CD19B-Cell Activation Factor ReceptorB-LymphocytesCD40 AntigensCell SurvivalInterleukin-4Intracellular Signaling Peptides and ProteinsLipopolysaccharidesMembrane GlycoproteinsMiceMice, KnockoutOligodeoxyribonucleotidesADP-ribosyl Cyclase 1AntibodiesAntigens, CDAntigens, CD19B-Cell Activation Factor ReceptorCd38 protein, mouseCD40 AntigensCPG-oligonucleotideInterleukin-4Intracellular Signaling Peptides and ProteinsLipopolysaccharidesLy78 protein, mouseMembrane GlycoproteinsOligodeoxyribonucleotidesPhosphatidylinositol 3-KinasesProtein-Tyrosine KinasesReceptors, Antigen, B-CellSyk KinaseSyk protein, mouseTnfrsf13c protein, mouseBAFF receptorB‐cell antigen receptorCD19mb1‐CreERT2Syk

Identifiers

PMID25630702
PMCPMC4388600
OpenAlexW2137269303

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.