Evidence map›Paper›PMID 40982212›Full record

ArticleHepatology communications2025

Age-associated B cells enhance tertiary lymphoid structures in the liver and promote HCC formation.

Anne E Morsing, Kenneth Green, Signe Clausen, Camilla R Benjaminsen, Mathilde S Blaavand, Julia K Demtröder, Johannes Skraep, Lisbeth Jensen, Peter Breining, Mads Kjolby and 3 more

Abstract read
In one paragraph

Article in Hepatology communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Review
  2. Review
  3. 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

13 authors.

Anne E MorsingDepartment of Biomedicine, Aarhus University, Aarhus, Denmark.
Kenneth GreenDepartment of Biomedicine, Aarhus University, Aarhus, Denmark.
Signe ClausenDepartment of Biomedicine, Aarhus University, Aarhus, Denmark.
Camilla R BenjaminsenDepartment of Biomedicine, Aarhus University, Aarhus, Denmark.
Mathilde S BlaavandDepartment of Biomedicine, Aarhus University, Aarhus, Denmark.
Julia K DemtröderDepartment of Biomedicine, Aarhus University, Aarhus, Denmark.
Johannes SkraepDepartment of Biomedicine, Aarhus University, Aarhus, Denmark.
Lisbeth JensenDepartment of Biomedicine, Aarhus University, Aarhus, Denmark.
Peter BreiningDepartment of Clinical Medicine, Aarhus University, Aarhus, Denmark.
Mads KjolbyDepartment of Biomedicine, Aarhus University, Aarhus, Denmark.
Mikkel VendelboDepartment of Biomedicine, Aarhus University, Aarhus, Denmark.
Søren E DegnDepartment of Biomedicine, Aarhus University, Aarhus, Denmark.
Martin K ThomsenDepartment of Biomedicine, Aarhus University, Aarhus, Denmark.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundHepatocellular carcinoma (HCC) is the sixth most common cancer worldwide, with chronic liver inflammation being a major risk factor. Tertiary lymphoid structures (TLS) have been associated with improved survival and better response to immune checkpoint inhibitors in several cancers. However, their role in HCC remains unclear, and findings are often contradictory.

methodsThe study investigated the presence and composition of TLSs across multiple liver disease models, including livers containing HCC. TLSs were characterized to identify the essential cellular components for functional lymphoid activity. The functional role of age-associated B cells (ABCs) was further explored by blocking T-bet expression in B cells, thereby preventing their differentiation into ABCs.

resultsTLS frequency was increased in livers containing HCC. Characterization confirmed the presence of key immune cell subsets supporting lymphoid function. Blocking T-bet in B cells led to a reduction in ABCs, which resulted in smaller TLS, a specific decrease in hepatic B cells, and reduced tumor lesion size in HCC-bearing mice.

conclusionsThese findings demonstrate that ABCs promote TLS formation and growth, facilitating B-cell recruitment to the liver and supporting HCC progression. Targeting T-bet-dependent ABC differentiation may represent a novel strategy to limit TLS formation and slow HCC progression.

Indexed as

B-LymphocytesCarcinoma, HepatocellularLiver NeoplasmsTertiary Lymphoid StructuresAge FactorsAnimalsDisease Models, AnimalHumansLiverMaleMiceMice, Inbred C57BLT-bet Transcription FactorT-Box Domain ProteinsT-bet Transcription FactorT-Box Domain ProteinsB cellshepatocellular carcinomamouse modeltertiary lymphoid structures

Identifiers

PMID40982212
PMCPMC12456604

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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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 Socratic graph.