Evidence map›Paper›PMID 41252283›Full record

ArticleCardiovascular research2025

Allogeneic haematopoietic cell transplantation promotes atherosclerosis in mice via CD8+ T cells.

Ivana Jorgacevic, Haroon Shaikh, Hla Ali, Maja Bundalo, Sarah Schäfer, Michael A G Kern, Maike Büttner-Herold, Simone Reu-Hofer, Clément Cochain, Hendrik Bartolomaeus and 13 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cardiovascular research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

23 authors.

Ivana JorgacevicInstitute of Experimental Biomedicine, University Hospital Würzburg, Josef-Schneider-Str. 2, D16, Würzburg 97080, Germany.
Haroon ShaikhDepartment of Internal Medicine II, University Hospital Würzburg, Würzburg, Germany.
Hla AliInstitute of Experimental Biomedicine, University Hospital Würzburg, Josef-Schneider-Str. 2, D16, Würzburg 97080, Germany.
Maja BundaloInstitute of Experimental Biomedicine, University Hospital Würzburg, Josef-Schneider-Str. 2, D16, Würzburg 97080, Germany.
Sarah SchäferInstitute of Experimental Biomedicine, University Hospital Würzburg, Josef-Schneider-Str. 2, D16, Würzburg 97080, Germany.ORCID 0000-0002-6053-0930
Michael A G KernDepartment of Internal Medicine II, University Hospital Würzburg, Würzburg, Germany.
Maike Büttner-HeroldDepartment of Nephropathology, Institute of Pathology, Friedrich-Alexander-University Erlangen-Nuremberg (FAU) and University Hospital, Erlangen, Germany.
Simone Reu-HoferInstitute of Pathology, Julius-Maximilians-University Würzburg, Würzburg, Germany.
Clément CochainInstitute of Experimental Biomedicine, University Hospital Würzburg, Josef-Schneider-Str. 2, D16, Würzburg 97080, Germany.
Hendrik BartolomaeusInstitute of Experimental Biomedicine, University Hospital Würzburg, Josef-Schneider-Str. 2, D16, Würzburg 97080, Germany.
Antoine-Emmanuel SalibaHelmholtz-Center for Infection Research (HZI), Helmholtz Institute for RNA-based Infection Research (HIRI), Würzburg, Germany.ORCID 0000-0001-8539-2784
Melanie RöschInstitute of Experimental Biomedicine, University Hospital Würzburg, Josef-Schneider-Str. 2, D16, Würzburg 97080, Germany.
Giuseppe RizzoInstitute of Experimental Biomedicine, University Hospital Würzburg, Josef-Schneider-Str. 2, D16, Würzburg 97080, Germany.
Estibaliz Arellano VieraDepartment of Internal Medicine II, University Hospital Würzburg, Würzburg, Germany.
Juan Gamboa VargasDepartment of Internal Medicine II, University Hospital Würzburg, Würzburg, Germany.
Friederike Berberich-SiebeltInstitute of Pathology, Julius-Maximilians-University Würzburg, Würzburg, Germany.
Wolfgang HerrDepartment of Internal Medicine III, University Hospital Regensburg, Regensburg, Germany.
Louis BoonJJP Biologics, Bobrowiecka 6, Warsaw 00-728, Poland.
Andreas RosenwaldInstitute of Pathology, Julius-Maximilians-University Würzburg, Würzburg, Germany.
Elke ButtInstitute of Experimental Biomedicine, University Hospital Würzburg, Josef-Schneider-Str. 2, D16, Würzburg 97080, Germany.
Heike M HermannsDepartment of Internal Medicine II, University Hospital Würzburg, Würzburg, Germany.
Andreas BeilhackDepartment of Internal Medicine II, University Hospital Würzburg, Würzburg, Germany.ORCID 0000-0002-3165-2648
Alma ZerneckeInstitute of Experimental Biomedicine, University Hospital Würzburg, Josef-Schneider-Str. 2, D16, Würzburg 97080, Germany.ORCID 0000-0001-8551-4729

Funding

Deutsche ForschungsgemeinschaftGerman Research Foundation 324392634-TR221German Research Foundation 453989101-SFB1525German Research Foundation ZE827/14-1
6 · The paper itself

Abstract

aimsPatients undergoing allogeneic haematopoietic cell transplantation (allo-HCT) are at a risk of developing graft-vs.-host disease (GvHD) and are afflicted with an increased incidence of cardiovascular events. Whether allo-HCT contributes to atherosclerosis progression has not been addressed experimentally. METHODS AND

resultsHere, we applied a novel minor histocompatibility antigen mismatch allo-HCT mouse model by transplanting C57BL/6 mice deficient for the LDL receptor (B6.Ldlr-/-) with bone marrow (BM) or BM and T cells (BMT) from BALB/b donors (BALB/b, H-2b → B6.Ldlr-/-, and H-2b), and feeding recipients a western diet. Mild clinical GvHD symptoms ensued with low disease activity in typical GvHD target organs. However, allogeneic BMT recipients developed increased atherosclerotic lesions compared with mice receiving BM only or syngeneic BMT recipients. Atherosclerotic lesions showed a heightened infiltration of effector CD8+ T cells in the aorta of BMT recipients. Furthermore, BMT recipients exhibited significantly higher serum cholesterol levels than BM-recipients. Notably, CD8+ T-cell depletion in B6.Ldlr-/- BMT recipients reduced atherosclerotic lesion formation and decreased cholesterol levels.

conclusionThese data may provide a novel mechanistic underpinning for the clinically observed increased incidence of cardiovascular disease in long-term allo-HCT survivors. Moreover, we have identified CD8+ T cells as potential targets for mitigating GvHD-induced atherosclerosis.

Indexed as

AortaAortic DiseasesAtherosclerosisCD8-Positive T-LymphocytesGraft vs Host DiseaseHematopoietic Stem Cell TransplantationAnimalsBone Marrow TransplantationCholesterolDisease Models, AnimalMaleMice, Inbred BALB CMice, Inbred C57BLMice, KnockoutPlaque, AtheroscleroticReceptors, LDLCholesterolReceptors, LDLAtherosclerosisGraft-versus-host diseaseHaematopoietic cell transplantationT cells

Identifiers

PMID41252283
PMCPMC12754844

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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.