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Systemic administration of CD28-deprived in vitro-induced regulatory T cell attenuates pathological remodeling caused by pressure overload-induced cardiac fibrosis

GSE300131 Mus musculus Expression profiling by high throughput sequencing 6 samples Submitted 2026/03/11 Platform GPL34290
Summary
In heart failure, myocardial fibrosis driven by immune-mediated inflammation contributes to progressive cardiac dysfunction. We investigated the therapeutic efficacy of CD28-deprived in vitro–induced regulatory T cells (iTreg), a stable Treg subset, in a murine model of pressure overload–induced heart failure. CD28-deprived iTreg were intravenously administered one week after transverse aortic constriction (TAC). Treated mice showed improved cardiac function, reduced ventricular fibrosis, and Treg localization in the heart. Transcriptomic analysis revealed downregulation of profibrotic and proinflammatory pathways, including TNF-α/NF-κB and TGF-β signaling. These findings suggest that systemic delivery of CD28-deprived iTreg effectively modulates the inflammatory microenvironment and suppresses cardiac remodeling, offering a promising immunomodulatory strategy for treating heart failure.
Published in
Stable and functional regulatory T cell attenuates fibrotic remodeling in heart failure
Taguchi T, Kawamura T, Mikami N et al. · Regenerative therapy 2026 · PMID 41798793 · doi:10.1016/j.reth.2026.101079
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Also filed as BioProject PRJNA1279091 and SRA study SRP593036. Searching any of these in the dataset finder brings you back here.

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