Evidence map›Paper›PMID 24614588›Full record

ReviewNature reviews. Rheumatology2014

The BAFF/APRIL system in SLE pathogenesis.

Fabien B Vincent, Eric F Morand, Pascal Schneider, Fabienne Mackay

Registry-linked trialOpen access · greenAbstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Rheumatology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05659407 (The BAFF-var Polymorphism as a Biomarker of Response to B-depletive Treatment in Patients Affected by Systemic Lupus Erythematosus and Rheumatoid Arthritis), which is not on this map. Cited by 235 papers, 7 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
235citing papers in PubMed, 7 pooled it
34.2field-weighted citation impact, top 1% 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.

NCT05659407 unknown statusnot on this mapstarted 2020, after this paper: background citation

The BAFF-var Polymorphism as a Biomarker of Response to B-depletive Treatment in Patients Affected by Systemic Lupus Erythematosus and Rheumatoid Arthritis: a Prospective Study

TypeobservationalSponsorUniversity of CagliariRan2020 to 2023Enrolled60ConditionsSystemic Lupus Erythematosus, Rheumatoid Arthritis, BLyS PolymorphismArmsBelimumab in SLE patients / Rituximab in RA patients
3 · Its place in the literature

Who cites it

235 citing papers in PubMed, 7 syntheses or guidelines pooled it, 431 citations in OpenAlex.

  1. Pooled it
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  8. IgA2Cell reports. Medicine · 2025
    Trial
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  12. InterferonFrontiers in immunology · 2020
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  15. Review
  16. Observational
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  20. Anti-CD19-engineered exosomes enable B cell-targeted anti-BAFF mRNA delivery to alleviate lupus progression.Molecular therapy : the journal of the American Society of Gene Therapy · 2026
    Article

175 more citing papers are in PubMed but not listed here.

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

4 authors at 1 institution in 1 country.

Fabien B VincentDepartment of Immunology, Monash University, Central Clinical School, Alfred Medical Research and Education Precinct (AMREP), 89 Commercial Road, Melbourne, Vic 3004, Australia.
Eric F MorandMonash University Centre for Inflammatory Diseases, Southern Clinical School, Monash Medical Centre, 246 Clayton Road, Clayton, Vic 3168, Australia.
Pascal SchneiderDepartment of Biochemistry, University of Lausanne, Boveresses 155, 1066 Epalinges, Switzerland.
Fabienne MackayDepartment of Immunology, Monash University, Central Clinical School, Alfred Medical Research and Education Precinct (AMREP), 89 Commercial Road, Melbourne, Vic 3004, Australia.
Monash University · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Systemic lupus erythematosus (SLE) is characterized by multisystem immune-mediated injury in the setting of autoimmunity to nuclear antigens. The clinical heterogeneity of SLE, the absence of universally agreed clinical trial end points, and the paucity of validated therapeutic targets have, historically, contributed to a lack of novel treatments for SLE. However, in 2011, a therapeutic monoclonal antibody that neutralizes the cytokine TNF ligand superfamily member 13B (also known as B-cell-activating factor of the TNF family [BAFF]), belimumab, became the first targeted therapy for SLE to have efficacy in a randomized clinical trial. Because of its specificity, the efficacy of belimumab provides an opportunity to increase understanding of SLE pathophysiology. Although belimumab depletes B cells, this effect is not as powerful as that of other B-cell-directed therapies that have not been proven efficacious in randomized clinical trials. In this article, therefore, we review results suggesting that neutralizing BAFF can have effects on the immune system other than depletion of B cells. We also identify aspects of the BAFF system for which data in relation to SLE are still missing, and we suggest studies to investigate the pathogenesis of SLE and ways to refine anti-BAFF therapies. The role of a related cytokine, TNF ligand superfamily member 13 (also known as a proliferation-inducing ligand [APRIL]) in SLE is much less well understood, and hence this review focuses on BAFF.

Indexed as

Antibodies, Monoclonal, HumanizedAutoimmunityB-Cell Activating FactorHumansImmunosuppressive AgentsLupus Erythematosus, SystemicTumor Necrosis Factor Ligand Superfamily Member 13Antibodies, Monoclonal, HumanizedB-Cell Activating FactorbelimumabImmunosuppressive AgentsTNFSF13 protein, humanTumor Necrosis Factor Ligand Superfamily Member 13

Identifiers

PMID24614588
OpenAlexW1982924102

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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.