Evidence map›Paper›PMID 39256626›Full record

ReviewNature reviews. Immunology2025

Towards a unifying model for B-cell receptor triggering.

Søren E Degn, Pavel Tolar

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing 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

24 citing papers in PubMed.

  1. Review
  2. Article
  3. Decoding IGLL5 Mutation-Mediated BCR Signaling: A Novel Mechanism of CD8Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
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  5. Review
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  10. Review
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  12. Review
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  15. Review
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  17. Review
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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

2 authors.

Søren E DegnLaboratory for Lymphocyte Biology, Department of Biomedicine, Aarhus University, Aarhus, Denmark. sdegn@biomed.au.dk.ORCID http://orcid.org/0000-0001-5409-045X
Pavel TolarInstitute of Immunity and Transplantation, Division of Infection and Immunity, University College London, London, UK.ORCID http://orcid.org/0000-0003-4693-7299

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Antibodies are exceptionally versatile molecules with remarkable flexibility in their binding properties. Their natural targets range from small-molecule toxins, across viruses of different sizes, to bacteria and large multicellular parasites. The molecular determinants bound by antibodies include proteins, peptides, carbohydrates, nucleic acids, lipids and even synthetic molecules that have never existed in nature. Membrane-anchored antibodies also serve as receptors on the surface of the B cells that produce them. Despite recent structural insights, there is still no unifying molecular mechanism to explain how antibody targets (antigens) trigger the activation of these B-cell receptors (BCRs). After cognate antigen encounter, somatic hypermutation and class-switch recombination allow BCR affinity maturation and immunoglobulin class-specific responses, respectively. This raises the fundamental question of how one receptor activation mechanism can accommodate a plethora of variant receptors and ligands, and how it can ensure that individual B cells remain responsive to antigen after somatic hypermutation and class switching. There is still no definite answer. Here we give a brief historical account of the different models proposed to explain BCR triggering and discuss their merit in the context of the current knowledge of the structure of BCRs, their dynamic membrane distribution, and recent biochemical and cell biological insights.

Indexed as

B-LymphocytesModels, ImmunologicalReceptors, Antigen, B-CellAnimalsAntigensHumansImmunoglobulin Class SwitchingLymphocyte ActivationAntigensReceptors, Antigen, B-Cell

Identifiers

What OpenQuestion holds

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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.