Evidence map›Paper›PMID 24945754›Full record

ArticlePloS one2014

High levels of SOX5 decrease proliferative capacity of human B cells, but permit plasmablast differentiation.

Mirzokhid Rakhmanov, Heiko Sic, Anne-Kathrin Kienzler, Beate Fischer, Marta Rizzi, Maximilian Seidl, Kerstina Melkaoui, Susanne Unger, Luisa Moehle, Nadine E Schmit and 11 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
0.5field-weighted citation impact, top 34% 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

18 citing papers in PubMed, 39 citations in OpenAlex.

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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

21 authors at 4 institutions in 3 countries.

Mirzokhid RakhmanovCenter for Chronic Immunodeficiency (CCI), University Medical Center and University Freiburg, Freiburg, Germany.
Heiko SicCenter for Chronic Immunodeficiency (CCI), University Medical Center and University Freiburg, Freiburg, Germany.
Anne-Kathrin KienzlerCenter for Chronic Immunodeficiency (CCI), University Medical Center and University Freiburg, Freiburg, Germany.
Beate FischerCenter for Chronic Immunodeficiency (CCI), University Medical Center and University Freiburg, Freiburg, Germany.
Marta RizziCenter for Chronic Immunodeficiency (CCI), University Medical Center and University Freiburg, Freiburg, Germany.
Maximilian SeidlCenter for Chronic Immunodeficiency (CCI), University Medical Center and University Freiburg, Freiburg, Germany.
Kerstina MelkaouiCenter for Chronic Immunodeficiency (CCI), University Medical Center and University Freiburg, Freiburg, Germany.
Susanne UngerCenter for Chronic Immunodeficiency (CCI), University Medical Center and University Freiburg, Freiburg, Germany.
Luisa MoehleCenter for Chronic Immunodeficiency (CCI), University Medical Center and University Freiburg, Freiburg, Germany.
Nadine E SchmitCenter for Chronic Immunodeficiency (CCI), University Medical Center and University Freiburg, Freiburg, Germany.
Sachin D DeshmukhCenter for Chronic Immunodeficiency (CCI), University Medical Center and University Freiburg, Freiburg, Germany.
Cemil Korcan AyataDepartment of Pneumology, University Medical Center and University Freiburg, Freiburg, Germany.
Wolfgang SchuhDivision of Molecular Immunology, Department of Internal Medicine III, Nikolaus Fiebiger Center, University of Erlangen-Nürnberg, Erlangen, Germany.
Zhibing ZhangDepartment of Obstetrics and Gynecology, Virginia Commonwealth University, Richmond, Virginia, United States of America.
François-Loic CossetCIRI, INSERM U1111, EVIR, Ecole Normale Supérieure de Lyon, Université de Lyon, Lyon, France.
Els VerhoeyenCIRI, INSERM U1111, EVIR, Ecole Normale Supérieure de Lyon, Université de Lyon, Lyon, France; INSERM U1065, C3M, Metabolic control of cell deaths, Nice, France.
Hans-Hartmut PeterCenter for Chronic Immunodeficiency (CCI), University Medical Center and University Freiburg, Freiburg, Germany; Division of Rheumatology and Clinical Immunology, University Medical Center Freiburg, Freiburg, Germany.
Reinhard E VollCenter for Chronic Immunodeficiency (CCI), University Medical Center and University Freiburg, Freiburg, Germany; Division of Rheumatology and Clinical Immunology, University Medical Center Freiburg, Freiburg, Germany.
Ulrich SalzerCenter for Chronic Immunodeficiency (CCI), University Medical Center and University Freiburg, Freiburg, Germany; Division of Rheumatology and Clinical Immunology, University Medical Center Freiburg, Freiburg, Germany.
Hermann EibelCenter for Chronic Immunodeficiency (CCI), University Medical Center and University Freiburg, Freiburg, Germany; Division of Rheumatology and Clinical Immunology, University Medical Center Freiburg, Freiburg, Germany.
Klaus WarnatzCenter for Chronic Immunodeficiency (CCI), University Medical Center and University Freiburg, Freiburg, Germany; Division of Rheumatology and Clinical Immunology, University Medical Center Freiburg, Freiburg, Germany.
University Medical Center Freiburg · DEUniversité Claude Bernard Lyon 1 · FRFriedrich-Alexander-Universität Erlangen-Nürnberg · DEVirginia Commonwealth University · US

Funding

Dissection of the Structural Basis of MEIG1 in Assembling Sperm FlagellaR01HD076257 · NICHD · WAYNE STATE UNIVERSITY · PI ZHANG, ZHIBING · 2013 to 2017
$1.5M
NICHD NIH HHS HD076257NICHD NIH HHS R01 HD076257
6 · The paper itself

Abstract

Currently very little is known about the differential expression and function of the transcription factor SOX5 during B cell maturation. We identified two new splice variants of SOX5 in human B cells, encoding the known L-SOX5B isoform and a new shorter isoform L-SOX5F. The SOX5 transcripts are highly expressed during late stages of B-cell differentiation, including atypical memory B cells, activated CD21low B cells and germinal center B cells of tonsils. In tonsillar sections SOX5 expression was predominantly polarized to centrocytes within the light zone. After in vitro stimulation, SOX5 expression was down-regulated during proliferation while high expression levels were permissible for plasmablast differentiation. Overexpression of L-SOX5F in human primary B lymphocytes resulted in reduced proliferation, less survival of CD138neg B cells, but comparable numbers of CD138+CD38hi plasmablasts compared to control cells. Thus, our findings describe for the first time a functional role of SOX5 during late B cell development reducing the proliferative capacity and thus potentially affecting the differentiation of B cells during the germinal center response.

Indexed as

Cell DifferentiationAutoantigensCell Line, TumorCell ProliferationCells, CulturedGene Expression RegulationHumansLymphocyte ActivationPlasma CellsRNA, MessengerSOXD Transcription FactorsAutoantigensRNA, MessengerSOX13 protein, humanSOX5 protein, humanSOXD Transcription Factors

Identifiers

PMID24945754
PMCPMC4063782
OpenAlexW2084352820

What OpenQuestion holds

Textmetadata
LicenceCC BY
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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.