Gorczynski R M, Cohen Z, Fu X M, Levy G, Plapler H, Sullivan B
Department of Immunology, Toronto Hospital, Ontario, Canada.
Immunology. 1994 Sep;83(1):58-64.
Endothelial monolayers were prepared from neonatal heart or liver tissue of Lewis (Le) rats. Cells in their first passage of culture were used to investigate the short-term (1 hr at 37 degrees) binding of 51Cr-labelled Le rat lymphocytes prepared from the mesenteric lymph node (MLN), peripheral lymph node (PLN) or Peyer's patches (PP) to those endothelia, or the activation by concanavalin A (Con A) or irradiated (Lewis x Brown Norway)F1 (LBNF1), of Le cells on the monolayers after 84 hr in culture. MLN and PP showed preferential binding to, and activation on, liver endothelium compared with heart endothelium (approximately twofold difference), while the converse was seen with PLN. No inhibition of binding was seen with antibodies to intracellular adhesion molecule-1 (ICAM-1) or lymphocyte function-associated antigen-1 (LFA-1). Preincubation of endothelial cells with plasma isolated from the portal or hepatic vein of normal adult mice (5% plasma, 37 degrees for 14 hr) caused a 1.5-2-fold stimulation of binding of MLN/PP to heart endothelium, which was inhibited (> or = 75%) by anti-ICAM-1 or anti-LFA-1, and a fourfold stimulation of binding to liver endothelium, which was not inhibited by these monoclonal antibodies (< or = 25% inhibition). In contrast, antibodies to tumour necrosis factor-alpha (TNF-alpha) or interleukin-6 (IL-6) caused inhibition of activation of liver endothelium (> or = 75%), while producing little affect on activation of heart endothelium. Similar results were seen when lymphocyte activation on endothelial cells rather than adhesion cells was investigated. Our data suggest a heterogeneity in lymphocyte-endothelial interactions, which is further regulated, under physiological conditions, by the liver.
内皮单层细胞取自Lewis（Le）大鼠的新生心脏或肝脏组织。培养第一代的细胞用于研究从肠系膜淋巴结（MLN）、外周淋巴结（PLN）或派伊尔结（PP）制备的51Cr标记的Le大鼠淋巴细胞与这些内皮细胞的短期（37℃ 1小时）结合，或培养84小时后，单层细胞上的Le细胞被伴刀豆球蛋白A（Con A）或经辐照的（Lewis×Brown Norway）F1（LBNF1）激活的情况。与心脏内皮相比，MLN和PP对肝脏内皮表现出优先结合和激活（差异约为两倍），而PLN则相反。细胞间黏附分子-1（ICAM-1）或淋巴细胞功能相关抗原-1（LFA-1）抗体未观察到结合抑制。用从正常成年小鼠门静脉或肝静脉分离的血浆（5%血浆，37℃ 14小时）预孵育内皮细胞，导致MLN/PP与心脏内皮的结合增加1.5至2倍，这被抗ICAM-1或抗LFA-1抑制（≥75%），与肝脏内皮的结合增加四倍，而这些单克隆抗体对此无抑制作用（≤25%抑制）。相反，肿瘤坏死因子-α（TNF-α）或白细胞介素-6（IL-6）抗体导致肝脏内皮激活受到抑制（≥75%），而对心脏内皮激活影响很小。当研究淋巴细胞在内皮细胞而非黏附细胞上的激活时，也得到了类似结果。我们的数据表明淋巴细胞与内皮细胞相互作用存在异质性，在生理条件下，肝脏对此进一步发挥调节作用。
