Soluble domain 1 of platelet-endothelial cell adhesion molecule (PECAM) is sufficient to block transendothelial migration in vitro and in vivo.
Soluble domain 1 of platelet-endothelial cell adhesion molecule (PECAM) is sufficient to block transendothelial migration in vitro and in vivo.
复制标题
血小板 - 内皮细胞粘附分子（PECAM）的可溶性结构域1足以阻止体外和体内跨内皮迁移。
DOI：
10.1084/jem.185.7.1349
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发表时间：
1997-04-07
影响因子：
15.3
通讯作者：
Muller, W A
中科院分区：
文献类型：
--
作者：
Liao, F;Ali, J;Greene, T;Muller, W A
炎症反应涉及白细胞和内皮细胞的细胞粘附分子之间顺序的粘附相互作用。与之前的几个粘附步骤不同，跨内皮迁移（渗出），即白细胞在并列的内皮细胞之间迁移的步骤，似乎主要涉及一种粘附分子，即血小板-内皮细胞粘附分子（PECAM，CD 31）。因此，我们将PECAM作为肿瘤治疗的靶点。我们证明了由PECAM的整个细胞外部分或仅由PECAM的第一免疫球蛋白结构域与IgG的Fc部分融合制成的可溶性嵌合体在体外和体内阻断渗出。此外，截短形式的PECAM-IgG嵌合体不能稳定地结合其细胞配体。这提高了选择性抗PECAM疗法的可能性，其不会具有针对PECAM的抗体的不利调理或细胞活化特性。
The inflammatory response involves sequential adhesive interactions between cell adhesion molecules of leukocytes and the endothelium. Unlike the several adhesive steps that precede it, transendothelial migration (diapedesis), the step in which leukocytes migrate between apposed endothelial cells, appears to involve primarily one adhesion molecule, platelet–endothelial cell adhesion molecule (PECAM, CD31). Therefore, we have focused on PECAM as a target for antiinflammatory therapy. We demonstrate that soluble chimeras made of the entire extracellular portion of PECAM, or of only the first immunoglobulin domain of PECAM, fused to the Fc portion of IgG, block diapedesis in vitro and in vivo. Furthermore, the truncated form of the PECAM-IgG chimera does not bind stably to its cellular ligand. This raises the possibility of selective anti-PECAM therapies that would not have the untoward opsonic or cell-activating properties of antibodies directed against PECAM.