白癜风发病机制不明，CD8+T细胞介导的免疫损伤是黑素细胞(MC)破坏的主要效应环节，角质形成细胞线粒体活性氧簇（mtROS）可能参与启动这一过程，但机制不清。我们一直致力于mtROS与白癜风发病机制的研究，近来发现角质形成细胞mtROS可诱导趋化因子CXCL16表达，促进CD8+T细胞迁移，同时还发现皮损局部IL-1β升高。最新研究表明，mtROS可激活NLRP3炎症小体，释放IL-1β，促进抗原提呈、T细胞趋化及效应功能，提示NLRP3炎症小体可能是mtROS激活CD8+T细胞介导的免疫损伤的关键环节。然而，NLRP3炎症小体如何影响白癜风的发生和发展，亟待阐明；此外，NLRP3炎症小体在白癜风mtROS作用下激活免疫反应的分子机制，也是尚待明确的重要问题。因此，本研究拟在分子、细胞、组织和动物水平系统阐释mtROS激活NLRP3炎症小体促进MC免疫杀伤的具体机制，丰富白癜风发病机制。

Vitiligo is characterized by depigmention as a consequence of local melanocyte loss. Despite the fact that its etiology is not fully understood, vitiligo is believed to be caused by an autoimmune-mediated destruction of epidermal melanocytes mediated by CD8+T cells, which is triggered by excessive mitochondria reactive oxygen species (mtROS) in keratinocyte. However, how the mtROS trigger the autoimmune process remains unclear. Our previous data show that mtROS in keratinocytes could induce chemokine CXCL16 expression and contribute to skin recruitment of CD8+T cells in vitiligo, accompanied by upregulation of IL-1β. These data,together with latest reported studies suggested that NLRP3 inflammasome positively activited by mtROS leads to secretion of IL-1β and induces immune cell migration, consequently promoting antigen presentation and enhancing T cell effector function. Thus, NLRP3 inflammasome is undoubtedly a crucial factor which interacts mtROS and immune destruction. We therefore infer that mtROS may activate NLRP3 inflammasome and promote CD8+T cells to eradicate MC. This study aims to construct NLRP3 inflammasome activition/deficient model in vitro and in vivo, elucidating the mechanism of mtROS-autoimmunity-mediated melanocyte loss in vitiligo pathogenesis.