Hallmann R
Klinische Arbeitsgruppen für Rheumatologie der Max-Planck-Gesellschaft am Institut für experimentelle Medizin, Universität Erlangen-Nürnberg, Germany.
Behring Inst Mitt. 1993 Aug(92):138-43.
The adhesion of leukocytes to the endothelium is a hallmark in the development of an inflammation. Adhesion is caused by a number of mechanisms that depend upon the activation of the endothelium. The adhesion has to be specific for the different leukocyte types. I review here recent data with respect to polymorphonuclear granulocytes (PMN) adhesion to the endothelium of an inflammatory site. I especially focus on the pivotal role of Interferon gamma in the regulation of PMN adhesion to the endothelium. It modulates the adhesion of PMN caused by activation by other cytokines like IL-1, but does not affect the cell surface expression of the known adhesion molecules. I postulate the existence of a new class of cell surface modulators of adhesion which participate in the multiple step process of cell-cell adhesion.
白细胞与内皮细胞的黏附是炎症发展的一个标志。黏附是由多种依赖于内皮细胞激活的机制引起的。这种黏附对于不同类型的白细胞必须具有特异性。在此，我回顾了关于多形核粒细胞（PMN）与炎症部位内皮细胞黏附的最新数据。我特别关注干扰素γ在调节PMN与内皮细胞黏附方面的关键作用。它调节由其他细胞因子如IL-1激活所引起的PMN黏附，但不影响已知黏附分子的细胞表面表达。我推测存在一类新的细胞表面黏附调节剂，它们参与细胞间黏附的多步骤过程。
