Evidence map›Paper›PMID 28383107›Full record

ArticleEuropean journal of immunology2017

A mouse model of systemic lupus erythematosus responds better to soluble TACI than to soluble BAFFR, correlating with depletion of plasma cells.

Philipp Haselmayer, Michele Vigolo, Josquin Nys, Pascal Schneider, Henry Hess

Open access · hybridAbstract read
In one paragraph

Article in European journal of immunology, 2017. 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
2.0field-weighted citation impact, top 14% 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, 28 citations in OpenAlex.

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  6. Unique and redundant roles of mouse BCMA, TACI, BAFF, APRIL, and IL-6 in supporting antibody-producing cells in different tissues.Proceedings of the National Academy of Sciences of the United States of America · 2024
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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

5 authors at 2 institutions in 2 countries.

Philipp HaselmayerDepartment of Immunopharmacology, Immunology Translational Innovation Platform, Merck KGaA, Darmstadt, Germany.
Michele VigoloDepartment of Biochemistry, University of Lausanne, Epalinges, Switzerland.
Josquin NysDepartment of Biochemistry, University of Lausanne, Epalinges, Switzerland.
Pascal SchneiderDepartment of Biochemistry, University of Lausanne, Epalinges, Switzerland.ORCID 0000-0003-0677-9409
Henry HessDepartment of Immunopharmacology, Immunology Translational Innovation Platform, Merck KGaA, Darmstadt, Germany.
University of Lausanne · CHMerck (Germany) · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The TNF family cytokines B-cell activating factor (BAFF) and a proliferation-inducing ligand (APRIL) support plasma cell survival. It is known that inhibitors of BAFF only (BAFFR-Fc) or BAFF and APRIL (TACI-Fc) administered early enough in an NZB/NZW F1 mouse model of systemic lupus erythematosus (SLE) ameliorate clinical outcomes, pointing to a pathogenic role of BAFF. In the present study, TACI-Fc administrated at a later stage of disease, after onset of autoimmunity, decreased the number of bone marrow plasma cells and slowed down further formation of autoantibodies. TACI-Fc prevented renal damage during a 12-week treatment period regardless of autoantibody levels, while BAFFR-Fc did not despite a similar BAFF-blocking activity in vivo. TACI-Fc also decreased established plasma cells in a T-dependent hapten/carrier immunization system better than single inhibitors of BAFF or APRIL, and sometimes better than combined single inhibitors with at least equivalent BAFF and APRIL inhibitory activities. These results indicate that TACI-Fc can prevent symptoms of renal damage in a mouse model of SLE when BAFFR-Fc cannot, and point to a plasticity of plasma cells for survival factors. Targeting plasma cells with TACI-Fc might be beneficial to prevent autoantibody-mediated damages in SLE.

Indexed as

Disease Models, AnimalAnimalsAutoantibodiesAutoimmunityB-Cell Activating FactorB-Cell Activation Factor ReceptorB-LymphocytesFlow CytometryKidneyLupus Erythematosus, SystemicMicePlasma CellsTransmembrane Activator and CAML Interactor ProteinTumor Necrosis Factor Ligand Superfamily Member 13AutoantibodiesB-Cell Activating FactorB-Cell Activation Factor ReceptorTnfrsf13b protein, mouseTnfrsf13c protein, mouseTnfsf13b protein, mouseTnfsf13 protein, mouseTransmembrane Activator and CAML Interactor ProteinTumor Necrosis Factor Ligand Superfamily Member 13APRILBAFF/BLySLupusPlasma cellSLE

Identifiers

PMID28383107
PMCPMC5518279
OpenAlexW2605120829

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.