Evidence map›Paper›PMID 40397664›Full record

ArticleThe Journal of clinical investigation2025

Autophagy is an upstream mediator of chromatin dynamics in normal and autoimmune germinal center B cells.

Marta C Sallan, Filip Filipsky, Christina H Shi, Elena Pontarini, Manuela Terranova-Barberio, Gordon Beattie, Andrew Clear, Michele Bombardieri, Kevin Y Yip, Dinis Pedro Calado and 7 more

Abstract read
In one paragraph

Article in The Journal of clinical investigation, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing 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

5 citing papers in PubMed.

  1. A guide to B cell metabolism.Nature reviews. Immunology · 2026
    Review
  2. Review
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  5. Review
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

17 authors.

Marta C SallanBarts Cancer Institute, Queen Mary University of London, Charterhouse Square, London, United Kingdom.
Filip FilipskyBarts Cancer Institute, Queen Mary University of London, Charterhouse Square, London, United Kingdom.
Christina H ShiSanford Burnham Prebys Medical Discovery Institute, La Jolla, California, USA.
Elena PontariniCentre of Experimental Medicine and Rheumatology, William Harvey Research Institute, Charterhouse Square, London, United Kingdom.
Manuela Terranova-BarberioBarts Cancer Institute, Queen Mary University of London, Charterhouse Square, London, United Kingdom.
Gordon BeattieCRUK City of London Centre Single Cell Genomics Facility and.
Andrew ClearBarts Cancer Institute, Queen Mary University of London, Charterhouse Square, London, United Kingdom.
Michele BombardieriCentre of Experimental Medicine and Rheumatology, William Harvey Research Institute, Charterhouse Square, London, United Kingdom.
Kevin Y YipSanford Burnham Prebys Medical Discovery Institute, La Jolla, California, USA.
Dinis Pedro CaladoImmunity and Cancer Laboratory, Francis Crick Institute, London, United Kingdom.
Mark S CraggCentre for Cancer Immunology, Faculty of Medicine, University of Southampton, Southampton, United Kingdom.
Sonya JamesCentre for Cancer Immunology, Faculty of Medicine, University of Southampton, Southampton, United Kingdom.
Mathew CarterCentre for Cancer Immunology, Faculty of Medicine, University of Southampton, Southampton, United Kingdom.
Jessica OkosunBarts Cancer Institute, Queen Mary University of London, Charterhouse Square, London, United Kingdom.
John G GribbenBarts Cancer Institute, Queen Mary University of London, Charterhouse Square, London, United Kingdom.
Tanya KlymenkoSchool of Biological and Behavioural Sciences, Queen Mary University of London, London, United Kingdom.
Andrejs BraunBarts Cancer Institute, Queen Mary University of London, Charterhouse Square, London, United Kingdom.

Funding

Wellcome Trust FC001057
6 · The paper itself

Abstract

Germinal center (GC) B cells are pivotal in establishing a robust humoral immune response and long-term serological immunity while maintaining antibody self-tolerance. GC B cells rely on autophagy for antigen presentation and homeostatic maintenance. However, these functions, primarily associated with the light zone, cannot explain the spatiotemporal autophagy upregulation in the dark zone of GCs. Here, combining imaging, molecular, and genomic approaches, we defined a functional mechanism controlling chromatin accessibility in GC B cells during their dark zone transition. This mechanism links autophagy and nuclear lamin B1 dynamics with their downstream effects, including somatic hypermutation and antibody affinity maturation. Moreover, the autophagy-lamin B1 axis is highly active in the aberrant ectopic GCs in the salivary glands of Sjögren's disease, defining its role in autoimmunity.

Indexed as

AutoimmunityAutophagyB-LymphocytesChromatinGerminal CenterAnimalsHumansLamin Type BMiceSjogren's SyndromeChromatinLamin Type BAutoimmune diseasesAutoimmunityAutophagyCell biologyImmunology

Identifiers

PMID40397664
PMCPMC12208547

What OpenQuestion holds

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LicenceCC BY
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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.