ArticleJournal of advanced research2026
Treatment of clonal hematopoiesis associated atherosclerosis via vaccine-based clearance of the mutant cells.
Article in Journal of advanced research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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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.
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.
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Who cites it
1 citing paper in PubMed.
- Immuno-inflammatory-metabolic interactions in cardiovascular diseases: a review from basic mechanisms to clinical translation.Frontiers in immunology · 2026Review
Corrections and comments
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Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionClonal hematopoiesis of indeterminate potential (CHIP), driven by somatic mutations (e.g., TET2), is an independent risk factor for atherosclerosis (AS). CHIP-mutant macrophages promote plaque inflammation, but targeted therapies are lacking. Crucially, whether these clones acquire immunogenic neoantigens-enabling immune clearance-remains unexplored.
objectiveTo investigate if Tet2-mutant cells in CHIP-associated AS develop immunogenic neoantigens and evaluate a neoantigen-targeting vaccine strategy.
methodsTet2 was edited in hematopoietic cells via CRISPR/Cas9 and transplanted into Ldlr
resultsTet2 deficiency exacerbated atherosclerosis (+72% plaque area) and systemic inflammation. DNA and RNA sequencing results identified 2 mutations showing high MHC-I binding affinity, suggesting neoantigenicity. GelVax vaccination reduced aortic plaque burden by 45%, selectively cleared Tet2-mutant macrophages in plaques, attenuated systemic cytokines (TNF-α, IL-1β) and improved plaque stability (↓ necrotic core, ↑ collagen). The protection was primarily CD8
conclusionTet2-mutant cells in CHIP-associated AS acquire immunogenic neoantigens. Leveraging these antigens via a hydrogel vaccine induces clone-specific CD8
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