Hematopoietic stem cells (HSCs) are routinely mobilized from the bone marrow (BM) to the blood circulation for clinical transplantation. However, the precise mechanisms by which individual stem cells exit the marrow are not understood. This study identified cell-extrinsic and molecular determinants of a mobilizable pool of blood-forming stem cells. We found that a subset of HSCs displays macrophage-associated markers on their cell surface. Although fully functional, these HSCs are selectively niche-retained as opposed to stem cells lacking macrophage markers, which exit the BM upon forced mobilization. Macrophage markers on HSCs could be acquired through direct transfer by trogocytosis, regulated by receptor tyrosine-protein kinase C-Kit (CD117), from BM-resident macrophages in mouse and human settings. Our study provides proof of concept that adult stem cells utilize trogocytosis to rapidly establish and activate function-modulating molecular mechanisms.

中文翻译：

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C-Kit 相关的吞噬作用对造血干细胞库的调节


造血干细胞（HSC）通常从骨髓（BM）动员到血液循环中进行临床移植。然而，个体干细胞离开骨髓的确切机制尚不清楚。这项研究确定了可动员的造血干细胞池的细胞外在和分子决定因素。我们发现 HSC 的一个子集在其细胞表面显示巨噬细胞相关标记。尽管功能齐全，但这些 HSC 选择性地保留在生态位中，这与缺乏巨噬细胞标记的干细胞不同，巨噬细胞标记在强制动员时会离开 BM。 HSC 上的巨噬细胞标记物可以通过由受体酪氨酸蛋白激酶 C-Kit (CD117) 调节的 trogocytosis 直接转移从小鼠和人类环境中的 BM 驻留巨噬细胞获得。我们的研究提供了成体干细胞利用吞噬作用快速建立和激活功能调节分子机制的概念证明。