Evidence map›Paper›PMID 30524439›Full record

ArticleFrontiers in immunology2018

Inhibition of Membrane-Bound BAFF by the Anti-BAFF Antibody Belimumab.

Christine Kowalczyk-Quintas, Dehlia Chevalley, Laure Willen, Camilla Jandus, Michele Vigolo, Pascal Schneider

Open access · goldAbstract read
PubMed Full text at PMC Publisher
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 21 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 1 pooled it
3.8field-weighted citation impact, top 6% 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

21 citing papers in PubMed, 1 synthesis or guideline pooled it, 35 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Article
  5. Review
  6. Review
  7. Review
  8. Review
  9. Aberrant B-Cell Activation in Systemic Lupus Erythematosus.Kidney diseases (Basel, Switzerland) · 2022
    Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Targeting co-stimulatory molecules in autoimmune disease.Nature reviews. Drug discovery · 2020
    Review
  19. Article
  20. Article
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

6 authors at 1 institution in 1 country.

Christine Kowalczyk-QuintasDepartment of Biochemistry, University of Lausanne, Lausanne, Switzerland.
Dehlia ChevalleyDepartment of Biochemistry, University of Lausanne, Lausanne, Switzerland.
Laure WillenDepartment of Biochemistry, University of Lausanne, Lausanne, Switzerland.
Camilla JandusDepartment of Oncology UNIL CHUV, University of Lausanne, Lausanne, Switzerland.
Michele VigoloDepartment of Biochemistry, University of Lausanne, Lausanne, Switzerland.
Pascal SchneiderDepartment of Biochemistry, University of Lausanne, Lausanne, Switzerland.
University of Lausanne · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

B cell activating factor of the TNF family (BAFF, also known as BLyS), a cytokine that regulates homeostasis of peripheral B cells, is elevated in the circulation of patients with autoimmune diseases such as systemic lupus erythematosus (SLE). BAFF is synthetized as a membrane-bound protein that can be processed to a soluble form after cleavage at a furin consensus sequence, a site that in principle can be recognized by any of the several proteases of the pro-protein convertase family. Belimumab is a human antibody approved for the treatment of SLE, often cited as specific for the soluble form of BAFF. Here we show in different experimental systems, including in a monocytic cell line (U937) that naturally expresses BAFF, that belimumab binds to membrane-bound BAFF with similar EC50 as the positive control atacicept, which is a decoy receptor for both BAFF and the related cytokine APRIL (a proliferation inducing ligand). In U937 cells, binding of both reagents was only detectable in furin-deficient U937 cells, showing that furin is the main BAFF processing protease in these cells. In CHO cells expressing membrane-bound BAFF lacking the stalk region, belimumab inhibited the activity of membrane-bound BAFF less efficiently than atacicept, while in furin-deficient U937 cells, belimumab inhibited membrane-bound BAFF and residual soluble BAFF as efficiently as atacicept. These reagents did not activate complement or antibody-dependent cell cytotoxicity upon binding to membrane-bound BAFF

Indexed as

Antibodies, Monoclonal, HumanizedB-Cell Activating FactorCell MembraneFurinHEK293 CellsHumansLupus Erythematosus, SystemicTumor Necrosis Factor Ligand Superfamily Member 13U937 CellsAntibodies, Monoclonal, HumanizedB-Cell Activating FactorbelimumabFurinFURIN protein, humanTNFSF13B protein, humanTNFSF13 protein, humanTumor Necrosis Factor Ligand Superfamily Member 13antibody-dependent cell deathBAFFBLyScomplementfurinprotein shedding

Identifiers

PMID30524439
PMCPMC6256835
OpenAlexW2901141213

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.