Jagged-1+ Skin Tregs Modulate the Innate Immune Response to Wound Healing
June 2024
in “
Research Square (Research Square)
”
Studysummary This study demonstrated that in mice, the absence of Jagged-1 expression in skin-resident regulatory T cells significantly delays wound healing by reducing the accumulation of neutrophils, highlighting the role of Jagged-1 in coordinating immune cell recruitment during injury. Our plain-language summary of this paper — not a Tressless recommendation.
The study investigates the role of Jagged-1 (Jag1) in skin-resident regulatory T cells (Tregs) during wound healing. Using a tamoxifen inducible Foxp3creERT2Jag1fl/fl model, it was found that the absence of functional Jag1 in Tregs significantly delays wound closure. Unlike in hair regeneration, Jag1 in Tregs does not affect epithelial stem cells during wound healing but is crucial for the recruitment of Ly6G+ neutrophils to the wound site. The loss of Jag1 does not alter the abundance or activation of other immune cells like CD4+ and CD8+ T cells or pro-inflammatory macrophages. This indicates that Jag1-Notch signaling in Tregs is essential for coordinating innate cell recruitment during injury, highlighting its importance in effective wound repair.
