Tervaert J W, Kallenberg C G
Department of Clinical Immunology, University Hospital Groningen, The Netherlands.
Curr Opin Rheumatol. 1997 Jan;9(1):16-25. doi: 10.1097/00002281-199701000-00004.
Activation of the vascular endothelium by several different stimuli plays a crucial role in the initiation, localization, and propagation of vascular injury. In vitro studies have demonstrated that activation of cultured vascular endothelial cells renders them hyperadhesive for leukocytes. During the past decade it has become evident which cell adhesion molecules play a critical role in the interaction between the vascular endothelium and leukocytes in inflammation in general. Over the past year, advances have been made in understanding the interactions between leukocytes and vascular endothelial cells in vasculitis. Several studies have shown increased expression of adhesion molecules on circulating leukocytes and, in situ, in vasculitic lesions. Soluble adhesion molecules have appeared to be general nonspecific markers of endothelial activation. Hence, the clinical relevance of measuring soluble adhesion molecules is limited. Finally, the possibility of inhibiting adhesion molecule function in vivo remains an attractive therapeutic option in the vasculitides and is a focus of increasing research activity.
几种不同刺激对血管内皮的激活在血管损伤的起始、定位和扩散中起着关键作用。体外研究表明，培养的血管内皮细胞的激活使其对白细胞具有高粘附性。在过去十年中，哪些细胞粘附分子在一般炎症中血管内皮与白细胞之间的相互作用中起关键作用已变得很明显。在过去一年里，在理解血管炎中白细胞与血管内皮细胞之间的相互作用方面取得了进展。几项研究表明，循环白细胞以及血管炎病变原位的粘附分子表达增加。可溶性粘附分子似乎是内皮激活的一般非特异性标志物。因此，测量可溶性粘附分子的临床相关性有限。最后，体内抑制粘附分子功能的可能性在血管炎中仍然是一个有吸引力的治疗选择，并且是研究活动日益关注的焦点。
