?
当前位置:澳门黄金赌城 > 小柯机器人 >详情
皮肤干细胞上的CD80在受伤时促进调节性T细胞的局部扩增
作者:小柯机器人 发布时间:2024/4/30 14:26:20

美国芝加哥大学Yuxuan Miao等研究人员合作发现,皮肤干细胞上的CD80在受伤时促进调节性T细胞的局部扩增,以便在炎症环境中协调修复。2024年4月26日,《免疫》杂志在线发表了这项成果。

研究人员表示,组织损伤后,上皮干细胞(SC)被动员起来进入伤口,然后它们将面临严酷的炎症环境,这可能会阻碍它们修复损伤的能力。

研究人员揭示了在这种炎症环境中保护皮肤SC的机制。对迁移到伤口部位的毛囊SC(HFSC)基因表达谱的表征揭示了免疫调节程序的激活,包括CD80、主要组织相容性复合体II类(MHCII)和CXC模体趋化因子配体5(CXCL5)的表达。在HFSC中缺失CD80会损害再上皮化,减少外周生成的Treg(pTreg)细胞的积累,并增加中性粒细胞在受伤皮肤中的浸润。

重要的是,在缺乏pTreg细胞的小鼠中也观察到了类似的伤口愈合缺陷。这些研究结果表明,在皮肤损伤后,HFSC会通过促进Treg细胞的局部扩增来建立一个临时的保护网络,从而使皮肤重新上皮化,同时仍会在这个微环境外引发炎症,直到屏障恢复为止。

附:英文原文

Title: CD80 on skin stem cells promotes local expansion of regulatory T cells upon injury to orchestrate repair within an inflammatory environment

Author: Jingyun Luan, Cynthia Truong, Aleksandra Vuchkovska, Weijie Guo, Jennifer Good, Bijun Liu, Audrey Gang, Nicole Infarinato, Katherine Stewart, Lisa Polak, Hilda Amalia Pasolli, Emma Andretta, Alexander Y. Rudensky, Elaine Fuchs, Yuxuan Miao

Issue&Volume: 2024-04-26

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.

DOI: 10.1016/j.immuni.2024.04.003

Source: https://www.cell.com/immunity/fulltext/S1074-7613(24)00208-5

期刊信息

Immunity:《免疫》,创刊于1994年。隶属于细胞出版社,最新IF:43.474
官方网址:https://www.cell.com/immunity/home
投稿链接:https://www.editorialmanager.com/immunity/default.aspx

?