Savage C O, Cooke S P
Vascular Biology Team, MRC Clinical Research Centre, Harrow, Middlesex, UK.
J Autoimmun. 1993 Apr;6(2):237-49. doi: 10.1006/jaut.1993.1021.
The critical role played by the vascular endothelium in the development of vasculitic disease will be discussed within this article, attention being focused on the pathogenesis of the primary vasculitides, particularly Wegener's granulomatosis, microscopic polyarteritis and Kawasaki disease. Under normal circumstances the endothelium constitutes a barrier to the efflux of plasma proteins into the extracellular tissues, serves to maintain an anti-coagulant environment and forms a platform upon which many important biological processes take place. Alteration of the balance of these functions by inflammatory mediators and cytokines leads to the formation of a pro-coagulant environment, fluid leakage and increased adhesivity of the endothelium for neutrophils and lymphocytes. Both neutrophils and lymphocytes have the capacity to damage the endothelium directly, by the secretion of oxygen radicals, enzymes and other cytotoxic molecules, or indirectly by the secretion of cytokines which may alter the biological properties of endothelial cells, a process called endothelial activation. The role played by antibodies to the endothelium and to neutrophil cytoplasm components in mediating vascular injury in systemic vasculitis is also discussed and, finally, injury precipitated by components of the coagulation/thrombotic system.
本文将讨论血管内皮在血管炎性疾病发展过程中所起的关键作用,重点关注原发性血管炎,尤其是韦格纳肉芽肿、显微镜下多血管炎和川崎病的发病机制。在正常情况下,内皮构成血浆蛋白外流至细胞外组织的屏障,维持抗凝环境,并形成许多重要生物过程发生的平台。炎症介质和细胞因子改变这些功能的平衡会导致促凝环境的形成、液体渗漏以及内皮对中性粒细胞和淋巴细胞的黏附性增加。中性粒细胞和淋巴细胞都有能力直接通过分泌氧自由基、酶和其他细胞毒性分子来损伤内皮,或间接通过分泌可能改变内皮细胞生物学特性的细胞因子来损伤内皮,这一过程称为内皮激活。本文还讨论了针对内皮和中性粒细胞胞质成分的抗体在介导系统性血管炎血管损伤中的作用,最后讨论了凝血/血栓形成系统成分引发的损伤。