Palmblad J E, Lerner R
Department of Medicine, Karolinska Institute, Stockholm Söder Hospital, Sweden.
Clin Exp Immunol. 1992 Nov;90(2):300-4. doi: 10.1111/j.1365-2249.1992.tb07946.x.
Leukotriene B4 (LTB4) induced an in vitro transient state of hyperadhesiveness in cultured human umbilical vein endothelial cells (HUVEC), leading to a 2.2-fold increase in the binding of neutrophil granulocytes (PMN), which was less than that conferred by platelet activating factor (PAF) though more than thrombin did (3.4- or 2.0-fold increases, respectively). This study concerns the role of the adhesive molecules CD18 and CD54 for the LTB4- (as well as thrombin- and PAF-) induced endothelial hyperadhesiveness. The MoAbs 60.3 (to the CD18 molecule on PMN) and 84H10 (to one epitope of CD54 on the HUVEC) blocked the adherence of PMN to LTB4-treated HUVEC, whereas MoAb LB-2 (directed at another CD54 epitope) failed to do so. MoAb 84H10 blocked 43% of the thrombin-induced hyperadhesiveness, whereas the PAF response was unaffected. Thus, LTB4-induced HUVEC hyperadhesiveness may therefore be related to a specific domain on the CD54 (or on an antigenically related molecule) as well as being dependent on CD18, whereas the involvement of CD54 was much less or non-existent for the thrombin and PAF responses, respectively.
白三烯B4(LTB4)可在体外诱导培养的人脐静脉内皮细胞(HUVEC)出现短暂的高黏附状态,使中性粒细胞(PMN)的黏附增加2.2倍,虽然该增加倍数低于血小板活化因子(PAF)所诱导的增加倍数,但高于凝血酶所诱导的增加倍数(分别为3.4倍或2.0倍)。本研究关注黏附分子CD18和CD54在LTB4(以及凝血酶和PAF)诱导的内皮细胞高黏附性中的作用。单克隆抗体60.3(针对PMN上的CD18分子)和84H10(针对HUVEC上CD54的一个表位)可阻断PMN与LTB4处理的HUVEC的黏附,而单克隆抗体LB - 2(针对CD54的另一个表位)则无此作用。单克隆抗体84H10可阻断43%的凝血酶诱导的高黏附性,而对PAF诱导的反应无影响。因此,LTB4诱导的HUVEC高黏附性可能与CD54(或抗原相关分子)上的一个特定结构域有关,且依赖于CD18,而对于凝血酶和PAF诱导的反应,CD54的参与程度分别低得多或不存在。