Evidence map›Paper›PMID 41133684›Full record

ArticleAntibodies (Basel, Switzerland)2025

Evaluating the Therapeutic Efficacy of an Anti-BAFF Receptor Antibody Using a Rheumatoid Arthritis Mouse Model.

Adi Aharon, Rachel Birnboim-Perach, Omer Grotto, Adi Amir, Daniel Diadko, Nitzan Beltran, Limor Nahary, Itai Benhar

Abstract read
In one paragraph

Article in Antibodies (Basel, Switzerland), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. 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

8 authors.

Adi AharonDepartment of Molecular Microbiology and Biotechnology, The Shmunis School of Biomedicine and Cancer Research, The George S. Wise Faculty of Life Sciences, Tel-Aviv University, Tel-Aviv 6997801, Israel.
Rachel Birnboim-PerachDepartment of Molecular Microbiology and Biotechnology, The Shmunis School of Biomedicine and Cancer Research, The George S. Wise Faculty of Life Sciences, Tel-Aviv University, Tel-Aviv 6997801, Israel.
Omer GrottoDepartment of Molecular Microbiology and Biotechnology, The Shmunis School of Biomedicine and Cancer Research, The George S. Wise Faculty of Life Sciences, Tel-Aviv University, Tel-Aviv 6997801, Israel.
Adi AmirDepartment of Molecular Microbiology and Biotechnology, The Shmunis School of Biomedicine and Cancer Research, The George S. Wise Faculty of Life Sciences, Tel-Aviv University, Tel-Aviv 6997801, Israel.
Daniel DiadkoDepartment of Molecular Microbiology and Biotechnology, The Shmunis School of Biomedicine and Cancer Research, The George S. Wise Faculty of Life Sciences, Tel-Aviv University, Tel-Aviv 6997801, Israel.
Nitzan BeltranDepartment of Pathology, Wolfson Medical Center, Holon 5822012, Israel.
Limor NaharyDepartment of Molecular Microbiology and Biotechnology, The Shmunis School of Biomedicine and Cancer Research, The George S. Wise Faculty of Life Sciences, Tel-Aviv University, Tel-Aviv 6997801, Israel.
Itai BenharDepartment of Molecular Microbiology and Biotechnology, The Shmunis School of Biomedicine and Cancer Research, The George S. Wise Faculty of Life Sciences, Tel-Aviv University, Tel-Aviv 6997801, Israel.ORCID 0000-0002-0824-7177

Funding

ISF grant No. 3667/21
6 · The paper itself

Abstract

backgroundRheumatoid arthritis (RA) is a chronic autoimmune disease characterized by joint inflammation that leads to tissue damage and disability. RA affects approximately 0.5-1% of the global population and is driven by a complex interplay of genetic susceptibility, environmental factors, and immune dysregulation. While biologic and targeted synthetic DMARDs improved RA treatment, they have limitations in efficacy, safety, and accessibility. B-cell-targeting therapies, such as anti-CD20, have shown effectiveness, but only with broad immunosuppression, which can increase infection risk and compromise humoral immunity. Therefore, there is an unmet need for more selective therapeutic strategies that modulate pathogenic immune pathways while preserving protective immune functions. It has been suggested that targeting the BAFF pathway may offer a more favorable therapeutic approach compared to targeting CD20.

objectivesIn this study, we evaluated the therapeutic potential of V3-46s mIgG2a, an anti-BAFF-R (BR3) antibody in a mouse RA model, hypothesizing that it would offer a more selective and effective strategy.

methodsWe expressed and purified four antibody variants and assessed their binding and neutralizing activity in vitro. V3-46s mIgG2a was selected for in vivo evaluation in a collagen-induced arthritis (CIA) model.

resultsTreatment with this antibody delayed disease onset and reduced arthritis severity, spleen index, and B-cell populations.

conclusionsThese findings highlight the potential of BAFF-R-targeting antibodies as a therapeutic approach for RA treatment. This preclinical work lays the groundwork for future development of BAFF-R blockade as a complementary or alternative strategy to current biologic treatments.

Indexed as

BAFF receptor (BAFF-R)collagen-induced arthritis (CIA) mouse modelneutralizing antibodyrheumatoid arthritis (RA)

Identifiers

PMID41133684
PMCPMC12551023

What Socratic 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 Socratic graph.