Evidence map›Paper›PMID 29515028›Full record

ArticleJCI insight2018

Impaired TLR9 responses in B cells from patients with systemic lupus erythematosus.

Vincent Gies, Jean-Nicolas Schickel, Sophie Jung, Aurélie Joublin, Salomé Glauzy, Anne-Marie Knapp, Anne Soley, Vincent Poindron, Aurélien Guffroy, Jin-Young Choi and 6 more

Open access · goldAbstract read
In one paragraph

Article in JCI insight, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

43 citing papers in PubMed, 62 citations in OpenAlex.

  1. Review
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  4. Article
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  6. Extrafollicular CD19Journal of translational autoimmunity · 2024
    Article
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  12. For whom the B(c)ell tolls: CXCL4 AIDs human autoimmunity.The Journal of experimental medicine · 2023
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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

16 authors at 4 institutions in 3 countries.

Vincent GiesCNRS UPR 3572 "Immunopathology and Therapeutic Chemistry"/Laboratory of Excellence Médalis, Institute of Molecular and Cellular Biology (IBMC), Strasbourg, France.
Jean-Nicolas SchickelDepartment of Immunobiology, Yale University School of Medicine, New Haven, Connecticut, USA.
Sophie JungCNRS UPR 3572 "Immunopathology and Therapeutic Chemistry"/Laboratory of Excellence Médalis, Institute of Molecular and Cellular Biology (IBMC), Strasbourg, France.
Aurélie JoublinCNRS UPR 3572 "Immunopathology and Therapeutic Chemistry"/Laboratory of Excellence Médalis, Institute of Molecular and Cellular Biology (IBMC), Strasbourg, France.
Salomé GlauzyDepartment of Immunobiology, Yale University School of Medicine, New Haven, Connecticut, USA.
Anne-Marie KnappCNRS UPR 3572 "Immunopathology and Therapeutic Chemistry"/Laboratory of Excellence Médalis, Institute of Molecular and Cellular Biology (IBMC), Strasbourg, France.
Anne SoleyCNRS UPR 3572 "Immunopathology and Therapeutic Chemistry"/Laboratory of Excellence Médalis, Institute of Molecular and Cellular Biology (IBMC), Strasbourg, France.
Vincent PoindronDepartment of Clinical Immunology and Internal Medicine, National Reference Center for Rare Autoimmune Diseases, University Hospital, Strasbourg, France.
Aurélien GuffroyCNRS UPR 3572 "Immunopathology and Therapeutic Chemistry"/Laboratory of Excellence Médalis, Institute of Molecular and Cellular Biology (IBMC), Strasbourg, France.
Jin-Young ChoiDepartment of Immunobiology, Yale University School of Medicine, New Haven, Connecticut, USA.
Jacques-Eric GottenbergCNRS UPR 3572 "Immunopathology and Therapeutic Chemistry"/Laboratory of Excellence Médalis, Institute of Molecular and Cellular Biology (IBMC), Strasbourg, France.
Jennifer H AnolikDepartment of Medicine, Division of Allergy, Immunology and Rheumatology, University of Rochester Medical Center, Rochester, New York, USA.
Thierry MartinCNRS UPR 3572 "Immunopathology and Therapeutic Chemistry"/Laboratory of Excellence Médalis, Institute of Molecular and Cellular Biology (IBMC), Strasbourg, France.
Pauline Soulas-SprauelCNRS UPR 3572 "Immunopathology and Therapeutic Chemistry"/Laboratory of Excellence Médalis, Institute of Molecular and Cellular Biology (IBMC), Strasbourg, France.
Eric MeffreDepartment of Immunobiology, Yale University School of Medicine, New Haven, Connecticut, USA.
Anne-Sophie KorganowCNRS UPR 3572 "Immunopathology and Therapeutic Chemistry"/Laboratory of Excellence Médalis, Institute of Molecular and Cellular Biology (IBMC), Strasbourg, France.
Centre National de la Recherche Scientifique · FRYale University · USHôpitaux Universitaires de Strasbourg · FRUniversity of Rochester Medical Center · US

Funding

Regulation of IgA class switching in the intestinal mucosaP01AI061093 · NIAID · MOUNT SINAI SCHOOL OF MEDICINE OF NYU · PI CUNNINGHAM-RUNDLES, CHARLOTTE · 2004 to 2021
$29.8M
IMMUNE RESPONSES IN LUPUSR37AR040072 · NIAMS · YALE UNIVERSITY · PI CRAFT, JOSEPH EDGAR · 2000 to 2025
$7.4M
Yale Rheumatic Diseases Research Core CenterP30AR053495 · NIAMS · YALE UNIVERSITY · PI CRAFT, JOSEPH EDGAR · 2007 to 2017
$7.0M
Loss of B Cell Tolerance in Rheumatoid ArthritisR01AI071087 · NIAID · YALE UNIVERSITY · PI MEFFRE, ERIC · 2006 to 2016
$4.3M
Yale Autoimmunity Center of ExcellenceU19AI082713 · NIAID · YALE UNIVERSITY · PI CHO, JUDY H. · 2009 to 2013
$3.6M
MOLECULAR CHARACTERIZATION OF THE SNRNP POLYPEPTIDESR01AR040072 · NIAMS · YALE UNIVERSITY · PI Joseph Edgar Craft · 1990 to 2026
$2.5M
NIAID NIH HHS P01 AI061093NIAID NIH HHS R01 AI071087NIAID NIH HHS U19 AI082713NIAMS NIH HHS P30 AR053495NIAMS NIH HHS R01 AR040072NIAMS NIH HHS R37 AR040072
6 · The paper itself

Abstract

B cells play a central role in systemic lupus erythematosus (SLE) pathophysiology but dysregulated pathways leading to a break in B cell tolerance remain unclear. Since Toll-like receptor 9 (TLR9) favors the elimination of autoreactive B cells in the periphery, we assessed TLR9 function in SLE by analyzing the responses of B cells and plasmacytoid dendritic cells (pDCs) isolated from healthy donors and patients after stimulation with CpG, a TLR9 agonist. We found that SLE B cells from patients without hydroxychloroquine treatment displayed defective in vitro TLR9 responses, as illustrated by the impaired upregulation of B cell activation molecules and the diminished production of various cytokines including antiinflammatory IL-10. In agreement with CD19 controlling TLR9 responses in B cells, decreased expression of the CD19/CD21 complex on SLE B cells was detected as early as the transitional B cell stage. In contrast, TLR7 function was preserved in SLE B cells, whereas pDCs from SLE patients properly responded to TLR9 stimulation, thereby revealing that impaired TLR9 function in SLE was restricted to B cells. We conclude that abnormal CD19 expression and TLR9 tolerogenic function in SLE B cells may contribute to the break of B cell tolerance in these patients.

Indexed as

AdultAgedAged, 80 and overAntigens, CD19AutoimmunityB-LymphocytesCells, CulturedCytokinesDendritic CellsFemaleHumansImmune ToleranceLupus Erythematosus, SystemicMaleMiddle AgedOligodeoxyribonucleotidesAntigens, CD19CD19 molecule, humanCR2 protein, humanCytokinesODN2006OligodeoxyribonucleotidesReceptors, Complement 3dTLR9 protein, humanToll-Like Receptor 9Autoimmune diseasesAutoimmunityB cellsImmunology

Identifiers

PMID29515028
PMCPMC5922279
OpenAlexW2792413515

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.