Department of Pathology, Northwestern University Feinberg School of Medicine, Chicago, Illinois 60611, USA.
Annu Rev Pathol. 2011;6:323-44. doi: 10.1146/annurev-pathol-011110-130224.
Neither the innate nor adaptive immune system "responds" unless leukocytes cross blood vessels. This process occurs through diapedesis, in which the leukocyte moves in an ameboid fashion through tightly apposed endothelial borders and, in some cases, through the endothelial cell itself. This review focuses on the active role of the endothelial cell in diapedesis. Several mechanisms play a critical role in transendothelial migration, including signals derived from clustering of apically disposed intercellular adhesion molecule 1 and vascular cell adhesion molecule 1, disruption or loosening of adherens junctions, and targeted recycling of platelet/endothelial cell adhesion molecule and other molecules from the recently described lateral border recycling compartment. Surprisingly, many of the same molecules and mechanisms that regulate paracellular migration also control transcellular migration. A hypothesis that integrates the various known mechanisms of transmigration is proposed.
固有免疫和适应性免疫系统都不会“作出反应”，除非白细胞穿过血管。这一过程通过血管渗出（diapedesis）发生，白细胞以阿米巴样方式穿过紧密贴合的内皮边界，在某些情况下，还穿过内皮细胞本身。本篇综述聚焦于内皮细胞在血管渗出中的主动作用。几种机制在跨内皮迁移中发挥关键作用，包括源自细胞间黏附分子 1 和血管细胞黏附分子 1 顶端聚集的信号、黏着连接的破坏或松动，以及血小板/内皮细胞黏附分子和其他分子从新近描述的侧边界再循环隔室的靶向再循环。令人惊讶的是，许多调节细胞旁迁移的相同分子和机制也控制细胞内迁移。提出了一个整合已知迁移各种机制的假说。
