Liesveld J L, Frediani K E, Harbol A W, DiPersio J F, Abboud C N
Department of Medicine, University of Rochester School of Medicine and Dentistry, NY.
Leukemia. 1994 Dec;8(12):2111-7.
The capacity of normal CD34+ marrow cells and CD34+ leukemic cell lines to adhere to human umbilical vein endothelial cells has been examined. Such interactions have importance since the processes of homing and egress within the marrow microenvironment involve the traverse of sinusoidal endothelium. Umbilical vein endothelial monolayers expressed CD44 and CD54 constitutively, and expression of both E-selectin (ELAM) and vascular cell adhesion molecule-1 (VCAM-1) were inducible with interleukin-1 (IL-1) alpha and beta and tumor necrosis factor (TNF). CD34+ marrow cells bound to unstimulated endothelial layers (33 vs. 16% to plastic), and their adhesion was significantly increased in the presence of IL-1 or TNF. This increased adhesion was not inhibited by functionally blocking antibodies to E-selectin or to CD54 but was partially inhibited by antibodies to VCAM. CD34+ KG1a cells also bound to endothelial monolayers (33 vs. 8% to plastic), and such adhesion was also upregulated by pretreatment of the endothelial cells with IL-1 or TNF. In contrast to normal CD34+ cells, this increased adhesion was inhibited by antibodies to E-selectin but not to VCAM. These findings indicate that adhesion of both normal CD34+ cells and leukemic blasts to endothelial cells can be upregulated by inflammatory mediators such as TNF and IL-1.
已对正常CD34⁺骨髓细胞和CD34⁺白血病细胞系与人脐静脉内皮细胞的黏附能力进行了检测。此类相互作用具有重要意义，因为骨髓微环境中的归巢和逸出过程涉及穿过窦状内皮。脐静脉内皮单层组成性表达CD44和CD54，并且E-选择素（ELAM）和血管细胞黏附分子-1（VCAM-1）的表达均可被白细胞介素-1（IL-1）α和β以及肿瘤坏死因子（TNF）诱导。CD34⁺骨髓细胞与未受刺激的内皮层结合（与塑料相比为33%对16%），并且在存在IL-1或TNF的情况下其黏附显著增加。这种增加的黏附不受针对E-选择素或CD54的功能阻断抗体的抑制，但部分受针对VCAM的抗体抑制。CD34⁺ KG1a细胞也与内皮单层结合（与塑料相比为33%对8%），并且通过用IL-1或TNF预处理内皮细胞，这种黏附也上调。与正常CD34⁺细胞相反，这种增加的黏附受针对E-选择素的抗体抑制，但不受针对VCAM的抗体抑制。这些发现表明，正常CD34⁺细胞和白血病母细胞与内皮细胞的黏附均可被TNF和IL-1等炎性介质上调。
