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非经典单核细胞清除外周血管树内皮细胞中的生长因子CSF1以确保存活和稳态
作者:小柯机器人 发布时间:2024/8/4 15:18:57

法国国家科研中心Marc Bajenoff团队近期取得重要工作进展,他们研究提出,非经典单核细胞清除外周血管树内皮细胞中的生长因子CSF1以确保存活和稳态。相关研究成果2024年7月31日在线发表于《免疫》杂志上。

据介绍,与占据特定组织位点的固着巨噬细胞不同,非经典单核细胞(NCM)是循环吞噬细胞,负责巡逻和清理血管腔表面,其特征是不断移动。

研究人员探讨了NCM培育生态位的性质。内皮细胞上生长因子CSF1的表达是NCM在血液中存活所必需的。缺乏内皮源性CSF1不影响血液CSF1浓度,表明NCM依赖于清除内皮细胞上存在的CSF1。内皮细胞上跨膜趋化因子和粘附因子CX3CL1的缺失会损害NCM的存活。

从机制上讲,内皮来源的CX3CL1和整合素亚基αL(ITGAL)促进了NCM对CSF1的摄取。CSF1由所有组织内皮细胞产生,除骨髓窦外,所有内皮细胞中Csf1的缺失都会损害NCM的存活,这支持一种模型,在这种模型中,完整的血管树充当NCM的生态位,其中存活和巡逻功能是相互关联的。

附:英文原文

Title: Non-classical monocytes scavenge the growth factor CSF1 from endothelial cells in the peripheral vascular tree to ensure survival and homeostasis

Author: Guilhem R. Thierry, Elisa M. Baudon, Mitchell Bijnen, Alicia Bellomo, Marine Lagueyrie, Isabelle Mondor, Louise Simonnet, Florent Carrette, Romain Fenouil, Sahar Keshvari, David A. Hume, David Dombrowicz, Marc Bajenoff

Issue&Volume: 2024-07-31

Abstract: Unlike sessile macrophages that occupy specialized tissue niches, non-classical monocytes (NCMs)—circulating phagocytes that patrol and cleanse the luminal surface of the vascular tree—are characterized by constant movement. Here, we examined the nature of the NCM’s nurturing niche. Expression of the growth factor CSF1 on endothelial cells was required for survival of NCMs in the bloodstream. Lack of endothelial-derived CSF1 did not affect blood CSF1 concentration, suggesting that NCMs rely on scavenging CSF1 present on endothelial cells. Deletion of the transmembrane chemokine and adhesion factor CX3CL1 on endothelial cells impaired NCM survival. Mechanistically, endothelial-derived CX3CL1 and integrin subunit alpha L (ITGAL) facilitated the uptake of CSF1 by NCMs. CSF1 was produced by all tissular endothelial cells, and deletion of Csf1 in all endothelial cells except bone marrow sinusoids impaired NCM survival, arguing for a model where the full vascular tree acts as a niche for NCMs and where survival and patrolling function are connected.

DOI: 10.1016/j.immuni.2024.07.005

Source: https://www.cell.com/immunity/fulltext/S1074-7613(24)00354-6

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