磷脂酶
磷脂酰丝氨酸
细胞生物学
吞噬作用
受体
小胶质细胞
巨噬细胞
细胞
细胞凋亡
突触修剪
生物
炎症
磷脂
免疫学
生物化学
体外
膜
出处
期刊:Nature Reviews Immunology
[Springer Nature]
日期:2019-04-24
卷期号:19 (9): 539-549
被引量:297
标识
DOI:10.1038/s41577-019-0167-y
摘要
Tissue macrophages rapidly recognize and engulf apoptotic cells. These events require the display of so-called eat-me signals on the apoptotic cell surface, the most fundamental of which is phosphatidylserine (PtdSer). Externalization of this phospholipid is catalysed by scramblase enzymes, several of which are activated by caspase cleavage. PtdSer is detected both by macrophage receptors that bind to this phospholipid directly and by receptors that bind to a soluble bridging protein that is independently bound to PtdSer. Prominent among the latter receptors are the MER and AXL receptor tyrosine kinases. Eat-me signals also trigger macrophages to engulf virus-infected or metabolically traumatized, but still living, cells, and this ‘murder by phagocytosis’ may be a common phenomenon. Finally, the localized presentation of PtdSer and other eat-me signals on delimited cell surface domains may enable the phagocytic pruning of these ‘locally dead’ domains by macrophages, most notably by microglia of the central nervous system. In this Review, Greg Lemke explains how macrophages are able to sense and respond to dead and dying cells. The author discusses the physiological implications of such macrophage activity.
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