The role of JAM-A and PECAM-1 in modulating leukocyte infiltration in inflamed and ischemic tissues
The role of JAM-A and PECAM-1 in modulating leukocyte infiltration in inflamed and ischemic tissues
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DOI：
10.1189/jlb.1105645
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发表时间：
2006-10-01
影响因子：
5.5
通讯作者：
Dejana, Elisabetta
中科院分区：
文献类型：
--
作者：
Nourshargh, Sussan;Krombach, Fritz;Dejana, Elisabetta
先天性和适应性免疫反应伴随着漏细胞粘附到血管壁以及它们随后浸润到下面的组织中。在大多数情况下，白细胞穿过内皮。通过挤压并置的内皮细胞的边界，这一过程被称为渗出。许多数据表明，蛋白质在内皮连接建立嗜同性的相互作用与相同的蛋白质，这是目前的白细胞。这些相互作用可能会引导白细胞通过内皮边界。本文主要综述了两种内皮连接蛋白[连接粘附分子-A（JAM-A）和PECAM]在白细胞渗出中的作用。用阻断抗体或灭活JAM-A和PECAM基因的体内数据表明，这两种蛋白质的作用取决于刺激和所用的实验模型。J. Leukoc. 80：714-718; 2006.
Innate and adaptive immunological responses are accompanied by leakocyte adhesion to the blood-vessel wall and their subsequent infiltration into the underlying tissues. In the majority of the cases, leukocytes cross the endothelium. by squeezing through the border of apposed endothelial cells, a process that is known as diapedesis. Many data suggest that proteins at endothelial junctions establish homophilic interactions with identical proteins, which are present on leukocytes. These interactions might then direct the passage of leukocytes through the endothelial border. In this review, we focus on two endothelial junctional proteins [junctional adhesion molecule-A (JAM-A) and PECAM], which play an important role in leukocyte diapedesis. In vivo data with blocking antibodies or inactivation of JAM-A and PECAM genes indicate that the role of these two proteins depends on the stimulus and the experimental model used. J. Leukoc. Biol. 80: 714-718; 2006.