Abstract：
Following tissue damage, epithelial stem cells (SCs) are mobilized to enter the wound, where they confront harsh inflammatory environments that can impede their ability to repair the injury. Here, we investigated the mechanisms that protect skin SCs within this inflammatory environment. Characterization of gene expression profiles of hair follicle SCs (HFSCs) that migrated into the wound site revealed activation of an immune-modulatory program, including expression of CD80, major histocompatibility complex class II (MHCII), and CXC motif chemokine ligand 5 (CXCL5). Deletion of CD80 in HFSCs impaired re-epithelialization, reduced accumulation of peripherally generated Treg (pTreg) cells, and increased infiltration of neutrophils in wounded skin. Importantly, similar wound healing defects were also observed in mice lacking pTreg cells. Our findings suggest that upon skin injury, HFSCs establish a temporary protective network by promoting local expansion of Treg cells, thereby enabling re-epithelialization while still kindling inflammation outside this niche until the barrier is restored.
摘要：
组织损伤后,动员上皮干细胞（SCs）进入伤口，在那里他们面临着恶劣的炎症环境，这可能会阻碍他们修复损伤的能力。这里,我们研究了在这种炎症环境中保护皮肤SCs的机制.迁移到伤口部位的毛囊SCs（HFSCs）的基因表达谱的表征揭示了免疫调节程序的激活，包括CD80的表达，主要组织相容性复合体II类（MHCII），和CXC基序趋化因子配体5(CXCL5)。CD80在HFSCs再上皮化受损中的缺失,减少外周生成的Treg（pTreg）细胞的积累，受伤皮肤的中性粒细胞浸润增加。重要的是,在缺乏pTreg细胞的小鼠中也观察到类似的伤口愈合缺陷。我们的研究结果表明，在皮肤损伤时，HFSCs通过促进Treg细胞的局部扩增来建立临时保护网络，从而使上皮重新形成，同时仍在该生态位之外点燃炎症，直到屏障恢复。
