Evidence map›Paper›PMID 40753161›Full record

ArticleNature communications2025

B cell maturation antigen (BCMA) is dispensable for the survival of long-lived plasma cells.

Shannon R Menzel, Edith Roth, Jens Wittner, Stefanie Brey, Leonie Weckwerth, Jana Thomas, Thomas H Winkler, Wolfgang Schuh, Hans-Martin Jäck, Katharina Pracht and 1 more

Abstract read
In one paragraph

Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing 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

12 citing papers in PubMed.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Why are long-lived plasma cells long-lived?Frontiers in immunology · 2026
    Review
  10. Review
  11. Review
  12. 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

11 authors.

Shannon R MenzelDivision of Molecular Immunology, Department of Medicine 3-Rheumatology and Immunology, Friedrich-Alexander-University Erlangen-Nürnberg, Erlangen, Germany.
Edith RothDivision of Molecular Immunology, Department of Medicine 3-Rheumatology and Immunology, Friedrich-Alexander-University Erlangen-Nürnberg, Erlangen, Germany.
Jens WittnerDivision of Molecular Immunology, Department of Medicine 3-Rheumatology and Immunology, Friedrich-Alexander-University Erlangen-Nürnberg, Erlangen, Germany.
Stefanie BreyDivision of Genetics, Department Biology, Nikolaus-Fiebiger-Center for Molecular Medicine, Friedrich-Alexander-University Erlangen-Nürnberg, Erlangen, Germany.
Leonie WeckwerthDivision of Molecular Immunology, Department of Medicine 3-Rheumatology and Immunology, Friedrich-Alexander-University Erlangen-Nürnberg, Erlangen, Germany.
Jana ThomasDivision of Molecular Immunology, Department of Medicine 3-Rheumatology and Immunology, Friedrich-Alexander-University Erlangen-Nürnberg, Erlangen, Germany.
Thomas H WinklerDivision of Genetics, Department Biology, Nikolaus-Fiebiger-Center for Molecular Medicine, Friedrich-Alexander-University Erlangen-Nürnberg, Erlangen, Germany.ORCID http://orcid.org/0000-0002-1860-0528
Wolfgang SchuhDivision of Molecular Immunology, Department of Medicine 3-Rheumatology and Immunology, Friedrich-Alexander-University Erlangen-Nürnberg, Erlangen, Germany.
Hans-Martin JäckDivision of Molecular Immunology, Department of Medicine 3-Rheumatology and Immunology, Friedrich-Alexander-University Erlangen-Nürnberg, Erlangen, Germany. hans-martin.jaeck@fau.de.ORCID http://orcid.org/0000-0002-6332-8463
Katharina Pracht *Division of Molecular Immunology, Department of Medicine 3-Rheumatology and Immunology, Friedrich-Alexander-University Erlangen-Nürnberg, Erlangen, Germany.ORCID http://orcid.org/0000-0002-8943-4897
Sebastian R Schulz *Division of Molecular Immunology, Department of Medicine 3-Rheumatology and Immunology, Friedrich-Alexander-University Erlangen-Nürnberg, Erlangen, Germany.

Funding

Deutsche Forschungsgemeinschaft (German Research Foundation) TRR130
6 · The paper itself

Abstract

The survival of antibody-secreting plasma cells is essential for long-lasting humoral immunity. BCMA is proposed to promote APRIL-mediated survival signals. However, extensive shedding of murine BCMA raises doubts about its role as a signaling receptor. To unequivocally establish BCMA's function in plasma cell survival, we generate two BCMA-deficient mouse lines and examine antigen-specific plasma cells post-immunization. Contrary to previous reports, both BCMA-deficient mouse lines have comparable numbers of antigen-specific long-lived plasma cells following both protein and mRNA immunizations. Transcriptome analysis reveals no reduction in survival signaling upon BCMA deletion. Interestingly, BCMA-deficient mice show increased total plasma cell numbers in the bone marrow and mesenteric lymph nodes after boost immunizations. These results indicate that BCMA has no intrinsic role in maintaining long-lived plasma cells. Instead, we propose that BCMA's function is limited to acting as a soluble decoy receptor for APRIL, thereby fine-tuning the plasma cell population size by limiting survival factor availability. Our findings thus provide a strong argument against the APRIL-BCMA axis being a central mechanism for plasma cell longevity.

Indexed as

B-Cell Maturation AntigenPlasma CellsAnimalsB-Cell Activating FactorCell SurvivalImmunity, HumoralImmunizationLymph NodesMiceMice, Inbred C57BLMice, KnockoutSignal TransductionTumor Necrosis Factor Ligand Superfamily Member 13B-Cell Activating FactorB-Cell Maturation AntigenTnfsf13b protein, mouseTnfsf13 protein, mouseTumor Necrosis Factor Ligand Superfamily Member 13

Identifiers

PMID40753161
PMCPMC12318048

What OpenQuestion 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 OpenQuestion graph.