ArticleMolecular therapy. Methods & clinical development2024
Persistent tailoring of MSC activation through genetic priming.
Article in Molecular therapy. Methods & clinical development, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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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.
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Who cites it
4 citing papers in PubMed.
- Genetically Modified MSCs for Targeted Regeneration: Balancing Efficacy, Biosafety, and GMP Standardization.Cells · 2026Review
- PET/EVOH nonwoven fabrics supportRegenerative therapy · 2026Article
- From hPSCs to MSCs: differentiation strategies, pathways, and the emergence of common regulatory networks.Cellular & molecular biology letters · 2026Review
- Integrated multi-omics profiling reveals immune-related biomarkers and regulatory networks for early prediction of tuberculosis in type 2 diabetes mellitus.Frontiers in immunology · 2026Article
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13 authors.
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Abstract
Mesenchymal stem/stromal cells (MSCs) are an attractive platform for cell therapy due to their safety profile and unique ability to secrete broad arrays of immunomodulatory and regenerative molecules. Yet, MSCs are well known to require preconditioning or priming to boost their therapeutic efficacy. Current priming methods offer limited control over MSC activation, yield transient effects, and often induce the expression of pro-inflammatory effectors that can potentiate immunogenicity. Here, we describe a genetic priming method that can both selectively and sustainably boost MSC potency via the controlled expression of the inflammatory-stimulus-responsive transcription factor interferon response factor 1 (IRF1). MSCs engineered to hyper-express IRF1 recapitulate many core responses that are accessed by biochemical priming using the proinflammatory cytokine interferon-γ (IFN-γ). This includes the upregulation of anti-inflammatory effector molecules and the potentiation of MSC capacities to suppress T cell activation. However, we show that IRF1-mediated genetic priming is much more persistent than biochemical priming and can circumvent IFN-γ-dependent expression of immunogenic MHC class II molecules. Together, the ability to sustainably activate and selectively tailor MSC priming responses creates the possibility of programming MSC activation more comprehensively for therapeutic applications.
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Registered trials
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