摘要
Transmigration of leukocytes through venular walls into the inflamed tissues plays a central role in innate immune res- ponses against infection or injury. Trans- endothelial migration （TEM） was widely believed to be the final step in the process of leukocyte emigration into inflamed tissues. Leukocyte TEM is driven by large-scale, comlicated molecular interactions that allow leukocyte TEM to occur with minimal disruption to the complex and delicate structures of vessel walls.1,2 However, the molecu- lar mechanisms underlying the leukocyte
Transmigration of leukocytes through venular walls into the inflamed tissues plays a central role in innate immune res- ponses against infection or injury. Trans- endothelial migration （TEM） was widely believed to be the final step in the process of leukocyte emigration into inflamed tissues. Leukocyte TEM is driven by large-scale, comlicated molecular interactions that allow leukocyte TEM to occur with minimal disruption to the complex and delicate structures of vessel walls.1,2 However, the molecu- lar mechanisms underlying the leukocyte
