Department of Immunology, The Weizmann Institute of Science, Rehovot 7610001, Israel.
Department of Molecular Cell Biology, Sanquin Research and Landsteiner Laboratory, Academic Medical Center, University of Amsterdam, 1066 CX Amsterdam, The Netherlands.
Trends Immunol. 2017 Aug;38(8):606-615. doi: 10.1016/j.it.2017.05.002. Epub 2017 May 27.
Leukocyte transendothelial migration (TEM) takes place across micron-wide gaps in specific post-capillary venules generated by the transmigrating leukocyte. Because endothelial cells contain a dense cytoskeletal network, transmigrating leukocytes must overcome these mechanical barriers as they squeeze their nuclei through endothelial gaps and pores. Recent findings suggest that endothelial cells are not a passive barrier, and upon engagement by transmigrating leukocytes trigger extensive dynamic modifications of their actin cytoskeleton. Unexpectedly, endothelial contractility functions as a restrictor of endothelial gap enlargement rather than as a facilitator of gap formation as was previously suggested. In this review we discuss current knowledge regarding how accurately timed endothelial actin-remodeling events are triggered by squeezing leukocytes and coordinate leukocyte TEM while preserving blood vessel integrity.
白细胞穿越血管内皮细胞迁移（TEM）发生在由穿越的白细胞产生的特定的后微动脉毛细血管中的微米宽的间隙中。由于内皮细胞含有致密的细胞骨架网络，因此在穿过内皮细胞间隙和孔时，穿越的白细胞必须克服这些机械屏障。最近的研究结果表明，内皮细胞不是一个被动的屏障，并且在被穿越的白细胞结合后，它们会引发其肌动蛋白细胞骨架的广泛动态修饰。出乎意料的是，内皮细胞的收缩性作为内皮细胞间隙扩大的限制因素，而不是以前所认为的促进间隙形成的因素。在这篇综述中，我们讨论了当前关于内皮细胞肌动蛋白重塑事件如何被挤压的白细胞准确触发以及协调白细胞 TEM 同时保持血管完整性的知识。
