ArticleMolecular therapy : the journal of the American Society of Gene Therapy2025
Inflammatory modulation by cord blood stem cells prevented digit deformation in recessive dystrophic epidermolysis bullosa.
Article in Molecular therapy : the journal of the American Society of Gene Therapy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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Who cites it
1 citing paper in PubMed.
- Long-term cytokine exposure remodels the methylome and transcriptome of recessive dystrophic epidermolysis bullosa keratinocytes - a bioinformatic analysis.Frontiers in cell and developmental biology · 2026Article
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13 authors.
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Abstract
Recessive dystrophic epidermolysis bullosa (RDEB) is a hereditary dermal blistering disorder caused by mutations in the COL7A1 gene encoding type VII collagen (C7), which progressively results in poor wound healing, fibrosis, and pseudosyndactyly. Using a C7 hypomorphic mouse model of RDEB, we demonstrated that inflammation critically drives disease progression and identified potential mechanisms by which human cord blood derived unrestricted somatic stem cells (USSCs) exert therapeutic benefit. Systemic USSC administration significantly mitigated early paw edema and prevented digit disfigurement; such effects were associated with promotion of wound healing macrophages. USSCs also deposited C7 at the dermal-epidermal junction, significantly promoted survival, and improved locomotor activity. Importantly, USSC treatment modulated relative balance between interleukin (IL)-1α and IL-1 receptor antagonist (IL-1Ra), resulting in significantly reduced IL1α/IL1Ra ratios and attenuated NK-кB signaling. Mechanistically, in response to inflammatory cues, USSCs secreted multiple paracrine factors, including leukemia inhibitory factor (LIF), granulocyte-colony-stimulating factor, and prostaglandin E2 (PGE2). Among these, LIF emerged as a key immunomodulator, simultaneously suppressing IL-1α and enhancing IL-1Ra expression. These findings highlight a novel mechanism in how LIF modulates IL-1-driven inflammation and suggest the potential therapeutic benefit of using USSCs to treat patients with RDEB.
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