Volpes R, Van Den Oord J J, Desmet V J
Department of Pathology, University Hospital St. Rafaël, Catholic University of Leuven, Belgium.
Hepatology. 1992 Feb;15(2):269-75. doi: 10.1002/hep.1840150216.
Adhesion to and penetration through the sinusoidal vascular endothelium is a mandatory step for leukocyte migration and accumulation at sites of liver inflammation. This leukocyte trafficking is controlled by interactions between adhesion molecules on leukocytes and corresponding ligands on endothelial cells. We have analyzed the in situ distribution of two recently described vascular adhesion molecules (i.e., endothelial leukocyte adhesion molecule-1 and vascular cell adhesion molecule-1) and of the lymphocyte "homing" receptor cluster of differentiation antigen-44 in normal and inflamed liver biopsy specimens. Endothelial leukocyte adhesion molecule-1 and vascular cell adhesion molecule-1 were absent from normal liver tissue, but they were strongly expressed on sinusoidal lining cells in inflammatory liver disease. Endothelial leukocyte adhesion molecule-1 expression predominated diffusely throughout the liver parenchyma in acute hepatitis; in contrast, vascular cell adhesion molecule-1 was mainly expressed in areas of periportal and intralobular inflammation in chronic active and persistent hepatitis. The "homing" receptor cluster of differentiation antigen-44 was weakly expressed on scattered mononuclear cells and on sinusoidal lining cells in normal liver tissue, but it was strongly up-regulated on mononuclear inflammatory cells and sinusoidal lining cells in acute and chronic hepatitis. In addition, reactivity for the cluster of differentiation antigen-44 was found on the membranes of variously sized clusters of hepatocytes in biopsy specimens with acute hepatitis. De novo or up-regulated expression of these adhesion molecules on sinusoidal lining cells in inflamed liver biopsy specimens indicates that these cells actively modulate their phenotype in response to environmental factors, thus playing a key role in the recruitment of leukocytes in acute and chronic liver inflammation.
黏附于肝血窦血管内皮并穿越内皮是白细胞在肝脏炎症部位迁移和聚集的必要步骤。这种白细胞迁移是由白细胞上的黏附分子与内皮细胞上相应配体之间的相互作用所控制的。我们分析了两种最近描述的血管黏附分子（即内皮白细胞黏附分子-1和血管细胞黏附分子-1）以及淋巴细胞“归巢”受体分化抗原-44在正常和炎症性肝活检标本中的原位分布。正常肝组织中不存在内皮白细胞黏附分子-1和血管细胞黏附分子-1，但它们在炎症性肝病的肝血窦衬里细胞上强烈表达。在急性肝炎中，内皮白细胞黏附分子-1的表达在整个肝实质中弥漫性占主导；相比之下，血管细胞黏附分子-1主要在慢性活动性和持续性肝炎的汇管区和小叶内炎症区域表达。分化抗原-44的“归巢”受体在正常肝组织中散在的单核细胞和肝血窦衬里细胞上弱表达，但在急性和慢性肝炎的单核炎症细胞和肝血窦衬里细胞上强烈上调。此外，在急性肝炎活检标本中，不同大小的肝细胞簇膜上发现了对分化抗原-44簇的反应性。炎症性肝活检标本中肝血窦衬里细胞上这些黏附分子的从头表达或上调表明，这些细胞响应环境因素积极调节其表型，从而在急性和慢性肝脏炎症中白细胞募集过程中起关键作用。
