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Immunity ; 57(5): 1071-1086.e7, 2024 May 14.
Artigo em Inglês | MEDLINE | ID: mdl-38677291

RESUMO

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.


Assuntos
Antígeno B7-1 , Folículo Piloso , Inflamação , Pele , Células-Tronco , Linfócitos T Reguladores , Cicatrização , Animais , Linfócitos T Reguladores/imunologia , Camundongos , Cicatrização/imunologia , Pele/imunologia , Pele/lesões , Pele/patologia , Células-Tronco/imunologia , Células-Tronco/metabolismo , Inflamação/imunologia , Folículo Piloso/imunologia , Antígeno B7-1/metabolismo , Camundongos Endogâmicos C57BL , Camundongos Knockout , Reepitelização/imunologia , Movimento Celular/imunologia , Proliferação de Células
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