Michael Daniel, Grando Sergei A
Department of Dermatology, University of California, Davis, CA, USA.
Curr Dir Autoimmun. 2008;10:333-43. doi: 10.1159/000131753.
The mode of action of intravenous immunoglobulin (IVIg) is complex. An ongoing research continues to elaborate and identify novel mechanisms. Recent advances have demonstrated that IVIg has direct effect on keratinocytes, the target cells of autoimmune blistering diseases. IVIg protects keratinocytes from pathogenic autoantibodies by preventing the autoantibody-induced of apoptosis and oncosis. This anti-apoptotic action of IVIg helps explain how IVIg works in severe, life threatening dermatologic conditions that are resistant to traditional systemic treatments, such as toxic epidermal necrolysis and Stevens-Johnson syndrome. Thus, the actions of IVIg are varied and complex, and the primary mechanisms of action may be different in different diseases.
静脉注射免疫球蛋白（IVIg）的作用模式很复杂。正在进行的研究不断阐述并确定新的机制。最近的进展表明，IVIg对自身免疫性水疱病的靶细胞角质形成细胞有直接作用。IVIg通过防止自身抗体诱导的细胞凋亡和胀亡来保护角质形成细胞免受致病性自身抗体的影响。IVIg的这种抗凋亡作用有助于解释其在严重的、危及生命的、对传统全身治疗有抗性的皮肤病（如中毒性表皮坏死松解症和史蒂文斯-约翰逊综合征）中是如何发挥作用的。因此，IVIg的作用是多样且复杂的，其主要作用机制在不同疾病中可能有所不同。
