Sultan A M, Dunn C J, Willoughby D A
Inflammation. 1979 Jul;3(3):305-17. doi: 10.1007/BF00914188.
Material with leuckocyte migration inhibition (LMI) activity has been demonstrated in various types of nonimmunologically induced acute pleural inflammatory exudates. This activity is present in inflammatory cell-free exudate and appears to involved the deposition of fibrin around the migrating leukocyte, resulting in "cell-trapping." This is supported by the fact that removal or inhibition of fibrin formation leads to loss of exudate LMI activity. Both fibrinogen and complement as well as vitamin K-dependent clotting factors appear to be required for LMI activity. The mechanism involved in the LMI reaction and its significance in nonimmune and cell-mediated immune inflammation are discussed.
在各种非免疫诱导的急性胸膜炎性渗出物中已证实存在具有白细胞迁移抑制(LMI)活性的物质。这种活性存在于无炎症细胞的渗出物中,似乎与纤维蛋白在迁移白细胞周围的沉积有关,从而导致“细胞捕获”。纤维蛋白形成的去除或抑制会导致渗出物LMI活性丧失,这一事实支持了上述观点。LMI活性似乎需要纤维蛋白原、补体以及维生素K依赖性凝血因子。本文讨论了LMI反应所涉及的机制及其在非免疫和细胞介导的免疫炎症中的意义。