Claudy A
Dermatology Clinic, University Hospital, Hôpital Edouard-Herriot, 69437 Lyon Cedex 03, France.
Eur J Dermatol. 1998 Mar;8(2):75-9.
There is compelling animal and human experimental evidence that leukocytoclastic vasculitis is a hypersensitivity vasculitis, similar in nature to the experimental Arthus reaction. The immune complexes formed in antigen excess circulate until some event occurs that cause deposition in blood vessel walls. Adhesion molecules and cytokines released by endothelial cells and activated neutrophils represent a key factor in this process. The membrane attack complex of complement plays a significant role in altering the endothelial cell membrane integrity. Activated neutrophils release proteolytic enzymes, especially collagenases and elastases, along with free oxygen radicals that damage the vessel walls and the surrounding tissues. It remains uncertain whether antineutrophilic cytoplasmic antibodies, anti-endothelial antibodies and anti-cardiolipin antibodies are epiphenomena or are directly involved in the disease process. Apoptotic cell death mediated by the Fas/Bc12 system is a feature of leucocytoclastic vasculitis. In conclusion, the post-capillary venule is the active orchestrator of neutrophils in leukocytoclastic vasculitis which mediate a complex series of endothelial/leukocyte interactions.
有令人信服的动物和人体实验证据表明，白细胞破碎性血管炎是一种超敏性血管炎，本质上类似于实验性阿瑟斯反应。在抗原过剩情况下形成的免疫复合物会循环，直到发生某些事件导致其在血管壁沉积。内皮细胞和活化的中性粒细胞释放的黏附分子和细胞因子是这一过程中的关键因素。补体的膜攻击复合物在改变内皮细胞膜完整性方面起重要作用。活化的中性粒细胞释放蛋白水解酶，尤其是胶原酶和弹性蛋白酶，以及损伤血管壁和周围组织的游离氧自由基。抗中性粒细胞胞浆抗体、抗内皮细胞抗体和抗心磷脂抗体是附带现象还是直接参与疾病过程仍不确定。由Fas/Bc12系统介导的凋亡性细胞死亡是白细胞破碎性血管炎的一个特征。总之，在白细胞破碎性血管炎中，毛细血管后微静脉是中性粒细胞的活跃组织者，它们介导了一系列复杂的内皮细胞/白细胞相互作用。
