吞噬作用
趋化因子
细胞生物学
趋化性
骨髓
细胞凋亡
细胞损伤
CXCR4型
免疫学
趋化因子受体
炎症
生物
受体
化学
生物化学
作者
Jing Wang,Mokarram Hossain,Ajitha Thanabalasuriar,Matthias Gunzer,Cynthia J. Meininger,Paul Kubes
出处
期刊:Science
[American Association for the Advancement of Science (AAAS)]
日期:2017-10-06
卷期号:358 (6359): 111-116
被引量:365
标识
DOI:10.1126/science.aam9690
摘要
Neutrophils have been implicated as harmful cells in a variety of inappropriate inflammatory conditions where they injure the host, leading to the death of the neutrophils and their subsequent phagocytosis by monocytes and macrophages. Here we show that in a fully repairing sterile thermal hepatic injury, neutrophils also penetrate the injury site and perform the critical tasks of dismantling injured vessels and creating channels for new vascular regrowth. Upon completion of these tasks, they neither die at the injury site nor are phagocytosed. Instead, many of these neutrophils reenter the vasculature and have a preprogrammed journey that entails a sojourn in the lungs to up-regulate CXCR4 (C-X-C motif chemokine receptor 4) before entering the bone marrow, where they undergo apoptosis.
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