Evidence map›Paper›PMID 29599769›Full record

ArticleFrontiers in immunology2018

Trib1 Is Overexpressed in Systemic Lupus Erythematosus, While It Regulates Immunoglobulin Production in Murine B Cells.

Léa Simoni, Virginia Delgado, Julie Ruer-Laventie, Delphine Bouis, Anne Soley, Vincent Heyer, Isabelle Robert, Vincent Gies, Thierry Martin, Anne-Sophie Korganow and 2 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.7field-weighted citation impact, top 33% 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

4 citing papers in PubMed, 11 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
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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

12 authors at 5 institutions in 1 country.

Léa SimoniCNRS UPR 3572 "Immunopathology and Therapeutic Chemistry"/Laboratory of Excellence Medalis, Institute of Molecular and Cellular Biology (IBMC), Strasbourg, France.
Virginia DelgadoCNRS UPR 3572 "Immunopathology and Therapeutic Chemistry"/Laboratory of Excellence Medalis, Institute of Molecular and Cellular Biology (IBMC), Strasbourg, France.
Julie Ruer-LaventieCNRS UPR 3572 "Immunopathology and Therapeutic Chemistry"/Laboratory of Excellence Medalis, Institute of Molecular and Cellular Biology (IBMC), Strasbourg, France.
Delphine BouisCNRS UPR 3572 "Immunopathology and Therapeutic Chemistry"/Laboratory of Excellence Medalis, Institute of Molecular and Cellular Biology (IBMC), Strasbourg, France.
Anne SoleyCNRS UPR 3572 "Immunopathology and Therapeutic Chemistry"/Laboratory of Excellence Medalis, Institute of Molecular and Cellular Biology (IBMC), Strasbourg, France.
Vincent HeyerInstitut de Génétique et de Biologie Moléculaire et Cellulaire (IGBMC), Illkirch, France.
Isabelle RobertInstitut de Génétique et de Biologie Moléculaire et Cellulaire (IGBMC), Illkirch, France.
Vincent GiesCNRS UPR 3572 "Immunopathology and Therapeutic Chemistry"/Laboratory of Excellence Medalis, Institute of Molecular and Cellular Biology (IBMC), Strasbourg, France.
Thierry MartinCNRS UPR 3572 "Immunopathology and Therapeutic Chemistry"/Laboratory of Excellence Medalis, Institute of Molecular and Cellular Biology (IBMC), Strasbourg, France.
Anne-Sophie KorganowCNRS UPR 3572 "Immunopathology and Therapeutic Chemistry"/Laboratory of Excellence Medalis, Institute of Molecular and Cellular Biology (IBMC), Strasbourg, France.
Bernardo Reina-San-MartinInstitut de Génétique et de Biologie Moléculaire et Cellulaire (IGBMC), Illkirch, France.
Pauline Soulas-SprauelCNRS UPR 3572 "Immunopathology and Therapeutic Chemistry"/Laboratory of Excellence Medalis, Institute of Molecular and Cellular Biology (IBMC), Strasbourg, France.
Institut de Biologie Moléculaire et Cellulaire · FRCentre National de la Recherche Scientifique · FRInstitut de génétique et de biologie moléculaire et cellulaire · FRUniversité de Strasbourg · FRInserm · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Systemic lupus erythematosus (SLE) is a severe and heterogeneous autoimmune disease with a complex genetic etiology, characterized by the production of various pathogenic autoantibodies, which participate in end-organ damages. The majority of human SLE occurs in adults as a polygenic disease, and clinical flares interspersed with silent phases of various lengths characterize the usual evolution of the disease in time. Trying to understand the mechanism of the different phenotypic traits of the disease, and considering the central role of B cells in SLE, we previously performed a detailed wide analysis of gene expression variation in B cells from quiescent SLE patients. This analysis pointed out an overexpression of

Indexed as

AdultAnimalsAntibody FormationAntigens, CDAntigens, Differentiation, B-LymphocyteAutoantibodiesAutoimmunityB-LymphocytesCells, CulturedFemaleHumansImmunoglobulin GImmunomodulationIntracellular Signaling Peptides and ProteinsLupus Erythematosus, SystemicMaleAntigens, CDAntigens, Differentiation, B-LymphocyteAutoantibodiesCD72 antigen, mouseImmunoglobulin GIntracellular Signaling Peptides and ProteinsProtein Serine-Threonine KinasesTRIB1 protein, humanB cellsIg secretionlupusmouse modelnegative regulatorTrib1

Identifiers

PMID29599769
PMCPMC5862796
OpenAlexW2791431414

What OpenQuestion holds

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Registered trials

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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.