Languino L R, Plescia J, Duperray A, Brian A A, Plow E F, Geltosky J E, Altieri D C
Scripps Research Institute, La Jolla, California 92037.
Cell. 1993 Jul 2;73(7):1423-34. doi: 10.1016/0092-8674(93)90367-y.
Leukocyte traffic in immune-inflammatory responses requires regulated adhesion of leukocyte subsets to vascular endothelium. We show that fibrinogen or normal human plasma enhances by 2- to 5-fold the adhesion of cells of myeloid and lymphoid lineage to endothelium. This mechanism is mediated by fibrinogen binding to complementary membrane receptors on leukocytes and endothelial cells. Using an affinity chromatography purification strategy, genetically engineered transfectants, and direct binding studies to the isolated recombinant protein, we identified a novel hematopoietic fibrinogen receptor participating in this adhesion pathway as intercellular adhesion molecule 1 (ICAM-1). Accordingly, a new model can be proposed, in which fibrinogen binding to a variety of vascular cell receptors mediates a specific pathway of cell to cell adhesion by bridging together leukocytes and endothelial cells.
白细胞在免疫炎症反应中的游走需要白细胞亚群与血管内皮细胞之间的黏附受到调控。我们发现,纤维蛋白原或正常人血浆可使髓系和淋巴系细胞与内皮细胞的黏附增强2至5倍。这一机制是由纤维蛋白原与白细胞和内皮细胞上的互补膜受体结合介导的。通过亲和层析纯化策略、基因工程转染细胞以及对分离出的重组蛋白进行直接结合研究,我们确定细胞间黏附分子1(ICAM-1)是参与这一黏附途径的一种新型造血纤维蛋白原受体。因此,可以提出一个新模型,其中纤维蛋白原与多种血管细胞受体的结合通过将白细胞和内皮细胞连接在一起,介导了一种特定的细胞间黏附途径。