Evidence map›Paper›PMID 42433156›Full record

ArticleCardiovascular research2026

Age-associated B cells predict coronary events in humans and aggravate murine atherosclerosis.

Jill de Mol, Pernilla Katra, Virginia Smit, Anna Witteveen, Lukas Tomas, Linda Andersson, Scott W M Engels, Samuel Andersson, Mireia N A Bernabé Kleijn, Alexandru Schiopu and 6 more

Abstract read
In one paragraph

Article in Cardiovascular research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

16 authors.

Jill de MolDivision of BioTherapeutics, Leiden Academic Centre for Drug Research (LACDR), Leiden University, Einsteinweg 55, Leiden 2333CC, The Netherlands.ORCID 0000-0003-3541-9912
Pernilla KatraDepartment of Clinical Sciences Malmö, Lund University, Malmö, Sweden.ORCID 0000-0002-5563-0494
Virginia SmitDivision of BioTherapeutics, Leiden Academic Centre for Drug Research (LACDR), Leiden University, Einsteinweg 55, Leiden 2333CC, The Netherlands.
Anna WitteveenDivision of BioTherapeutics, Leiden Academic Centre for Drug Research (LACDR), Leiden University, Einsteinweg 55, Leiden 2333CC, The Netherlands.
Lukas TomasDepartment of Medicine, LMU University Hospital, Munich, Germany.
Linda AnderssonDepartment of Clinical Sciences Malmö, Lund University, Malmö, Sweden.
Scott W M EngelsDivision of BioTherapeutics, Leiden Academic Centre for Drug Research (LACDR), Leiden University, Einsteinweg 55, Leiden 2333CC, The Netherlands.
Samuel AnderssonDepartment of Clinical Sciences Malmö, Lund University, Malmö, Sweden.
Mireia N A Bernabé KleijnDivision of BioTherapeutics, Leiden Academic Centre for Drug Research (LACDR), Leiden University, Einsteinweg 55, Leiden 2333CC, The Netherlands.
Alexandru SchiopuDepartment of Translational Medicine, Lund University, Malmö, Sweden.ORCID 0000-0002-7587-5050
Eva BengtssonDepartment of Clinical Sciences Malmö, Lund University, Malmö, Sweden.ORCID 0000-0001-7075-1772
Ilze BotDivision of BioTherapeutics, Leiden Academic Centre for Drug Research (LACDR), Leiden University, Einsteinweg 55, Leiden 2333CC, The Netherlands.ORCID 0000-0002-1242-1959
Daniel EngelbertsenDepartment of Clinical Sciences Malmö, Lund University, Malmö, Sweden.ORCID 0000-0002-0289-5210
Johan KuiperDivision of BioTherapeutics, Leiden Academic Centre for Drug Research (LACDR), Leiden University, Einsteinweg 55, Leiden 2333CC, The Netherlands.ORCID 0000-0001-5834-690X
Harry BjörkbackaDepartment of Clinical Sciences Malmö, Lund University, Malmö, Sweden.ORCID 0000-0003-3918-0857
Amanda C FoksDivision of BioTherapeutics, Leiden Academic Centre for Drug Research (LACDR), Leiden University, Einsteinweg 55, Leiden 2333CC, The Netherlands.ORCID 0000-0002-9747-3458

Funding

Albert Påhlsson FoundationDutch Heart Foundation 2018T051Dutch Heart Foundation 2019T067Dutch Heart Foundation 2019T107Dutch Research CouncilEuropean Union 101115159Fondation Leducq Network of ExcellenceMinistry of Research and Education of Romania PNRR-C9/I8-CF148Swedish governmental funding of clinical researchSwedish Heart Lung Foundation 20170617Swedish Heart Lung Foundation 20200760Swedish Heart Lung Foundation 20220293Swedish Research Council 2024-02632Swedish Research Council Dnr 2009-1039Swedish Research Council Dnr 2021-02942Swedish Research Council Dnr 349-2006237
6 · The paper itself

Abstract

aimsAging is a major risk factor for cardiovascular disease (CVD) and is also linked to a functional decline of the immune system. B cells contribute to atherosclerosis progression by antibody secretion, antigen presentation and T-cell regulation. During aging, CD11c+CD21low B cells accumulate, but it is unclear whether these age-associated B cells (ABCs) are linked with incident cardiovascular events in humans and if they contribute to the progression of atherosclerosis. METHODS AND

resultsTo investigate associations with first-time coronary events (CEs), circulating B cells were phenotyped with flow cytometry in a case-control study (N = 604) nested in the Malmö Diet and Cancer study cohort with a median of 14 years follow-up. Splenic B cells in young (5 months) and aged (21 months) female Ldlr-/- mice were characterized with single-cell RNA-sequencing coupled with B-cell receptor (BCR)-sequencing. Atherogenicity of ABCs was determined by adoptive transfer to Ldlr-/- and Ldlr-/-Rag1-/- mice. Compared with other B-cell populations, ABCs showed a significant positive correlation with age (Spearman's rho 0.24; P < 0.0001; across 46-68 years of age) and accumulated in aged atherosclerotic mice. CE cases had higher counts of ABCs than controls and regression analysis revealed an association with incident CEs, that was independent of cardiovascular risk factors [odds ratio: 1.92 (95% confidence interval 1.13-3.27), P = 0.016, comparing the fourth vs. first quartile]. Adoptive transfer of ABCs to recipient mice promoted atherosclerotic lesion development. In Ldlr-/- Rag1-/- mice, ABCs also increased necrotic cores (P < 0.05). B cells recovered from recipient mice after transfer expressed CD138 and secreted antibodies. In line with these findings, we demonstrated that ABCs expressed plasma cell (PC) differentiation genes and showed the greatest clonal expansion within the B-cell compartment, with extensive clonal overlap with PCs.

conclusionWe show that ABCs predict first-time CEs in humans and contribute to the immunopathology of atherosclerosis in mice, indicating that clonal expansion and accumulation of ABCs contribute to the strong association between age and CVD. ABCs may serve as potential prognostic and therapeutic targets for CVD.

Indexed as

AgingAtherosclerosisB-LymphocytesCoronary Artery DiseaseAdoptive TransferAdultAgedAge FactorsAnimalsCase-Control StudiesDisease Models, AnimalDisease ProgressionFemaleHomeodomain ProteinsHumansIncidenceHomeodomain ProteinsRAG-1 proteinReceptors, LDLAge-associated B cellsAgingAtherosclerosisCardiovascular disease

Identifiers

PMID42433156
PMCPMC13604844

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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.