Evidence map›Paper›PMID 21886837›Full record

ArticlePloS one2011

B cell signature during inactive systemic lupus is heterogeneous: toward a biological dissection of lupus.

Jean-Claude Garaud, Jean-Nicolas Schickel, Gilles Blaison, Anne-Marie Knapp, Doulaye Dembele, Julie Ruer-Laventie, Anne-Sophie Korganow, Thierry Martin, Pauline Soulas-Sprauel, Jean-Louis Pasquali

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed, 1 pooled it
2.4field-weighted citation impact, top 12% 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

34 citing papers in PubMed, 1 synthesis or guideline pooled it, 51 citations in OpenAlex.

  1. Pooled it
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  4. Aberrant B-Cell Activation in Systemic Lupus Erythematosus.Kidney diseases (Basel, Switzerland) · 2022
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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

10 authors at 6 institutions in 1 country.

Jean-Claude GaraudCNRS UPR 9021, Institut de Biologie Moléculaire et Cellulaire, Strasbourg, France.
Jean-Nicolas Schickel
Gilles Blaison
Anne-Marie Knapp
Doulaye Dembele
Julie Ruer-Laventie
Anne-Sophie Korganow
Thierry Martin
Pauline Soulas-Sprauel
Jean-Louis Pasquali
Centre National de la Recherche Scientifique · FRImmunologie, Immunopathologie et Chimie Thérapeutique · FRInstitut de Biologie Moléculaire et Cellulaire · FRHopitaux Civils de Colmar · FRInstitut de génétique et de biologie moléculaire et cellulaire · FRUniversité de Strasbourg · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Systemic lupus erythematosous (SLE) is an autoimmune disease with an important clinical and biological heterogeneity. B lymphocytes appear central to the development of SLE which is characterized by the production of a large variety of autoantibodies and hypergammaglobulinemia. In mice, immature B cells from spontaneous lupus prone animals are able to produce autoantibodies when transferred into immunodeficient mice, strongly suggesting the existence of intrinsic B cell defects during lupus. In order to approach these defects in humans, we compared the peripheral B cell transcriptomas of quiescent lupus patients to normal B cell transcriptomas. When the statistical analysis is performed on the entire group of patients, the differences between patients and controls appear quite weak with only 14 mRNA genes having a false discovery rate ranging between 11 and 17%, with 6 underexpressed genes (PMEPA1, TLR10, TRAF3IP2, LDOC1L, CD1C and EGR1). However, unforced hierarchical clustering of the microarrays reveals a subgroup of lupus patients distinct from both the controls and the other lupus patients. This subgroup has no detectable clinical or immunological phenotypic peculiarity compared to the other patients, but is characterized by 1/an IL-4 signature and 2/the abnormal expression of a large set of genes with an extremely low false discovery rate, mainly pointing to the biological function of the endoplasmic reticulum, and more precisely to genes implicated in the Unfolded Protein Response, suggesting that B cells entered an incomplete BLIMP1 dependent plasmacytic differentiation which was undetectable by immunophenotyping. Thus, this microarray analysis of B cells during quiescent lupus suggests that, despite a similar lupus phenotype, different biological roads can lead to human lupus.

Indexed as

Gene Expression RegulationB-LymphocytesCase-Control StudiesEndoplasmic ReticulumGene Expression ProfilingHumansInterleukin-4Lupus Erythematosus, SystemicMicroarray AnalysisPhenotypeUnfolded Protein ResponseInterleukin-4

Identifiers

PMID21886837
PMCPMC3160348
OpenAlexW2017138662

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.